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Yoshiro Saito

Section

Graduate School of Pharmaceutical Sciences

Job title

Professor

Degree

博士（薬学）（北海道大学）
修士（薬学）（北海道大学）

researchmap

https://researchmap.jp/SY004680_MBM

J-GLOBAL ID

201001036329322355

e-Rad No.

70357060

ORCID

https://orcid.org/0000-0002-0559-5889

Researcher ID

H-4597-2019

Research History 12

2022/12 - Present

Chiba University　Graduate School of Pharmaceutical Sciences
2018/09 - Present

東北大学大学院　薬学研究科　教授
2020/10 - 2025/03

University of Tokyo　Graduate School of Agricultural and Life Sciences　part-time lecturer
2018/04 - 2018/08

Doshisha University　Faculty of Life and Medical Sciences
2012/04 - 2018/03

Doshisha University　Faculty of Life and Medical Sciences
2008/04 - 2012/03

Doshisha University　Faculty of Life and Medical Sciences　Lecturer
2007/04 - 2008/03

AIST
2007 - 2008

Research Scientist for Human Stress Signal Research Center, National
2002/04 - 2007/03

産業技術総合研究所　ヒューマンストレスシグナル研究センター　若手任期付研究員
2002 - 2007

Research Scientist for Human Stress Signal Research Center, National
2000/01 - 2002/03

日本学術振興会　北海道大学大学院薬学研究科　特別研究員ＤＣ２
2001 - 2002

Postdoctoral Research Fellow of the Japan Society for the Promotion of Science

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Education 3

北海道大学大学院　薬学研究科　創薬化学専攻

1998/04 - 2001/03
北海道大学大学院　薬学研究科　薬学専攻

1996/04 - 1998/03
Hokkaido University　Faculty of Pharmaceutical Sciences

1991/04 - 1996/03

Committee Memberships 15

レドックスR&D戦略委員会　委員長

2025/04 - Present
日本微量元素学会　理事

2025/04 - Present
日本生化学会　代議員

2024/04 - Present
日本酸化ストレス学会　理事

2024/04 - Present
Japan Society for Biomedical Research on Trace Elements　delegate

2023/08 - Present
Redox Experimental Medicine　Editorial Board

2022/04 - Present
Japanese Society of Toxicology　councilor

2021/07 - Present
Free Radical Biology & Medicine　Editorial Board

2020/05 - Present
Journal of Clinical Biochemistry and Nutrition　Executive Editor

2020/01 - Present
Free Radical Research　Editorial Board

2019/02 - Present
日本薬学会　代議員

2019/02 - Present
日本脂質生化学会　幹事

2019/01 - Present
日本毒性学会生体金属部会　幹事

2018/11 - Present
ビタミンE研究会　幹事

2017/04 - Present
日本酸化ストレス学会　代議員

2014/04 - Present

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Professional Memberships 8

レドックスR&D戦略委員会

- Present
日本毒性学会

- Present
日本微量元素学会

- Present
日本酸化ストレス学会
日本薬学会
日本ビタミン学会
日本生化学会
The Japanese Biochemical Society

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Research Interests 10

Neurodegenerative disease
Diabetes
Biomarker
セレノプロテイン
細胞死
ストレス応答
酸化ストレス
Cell death
Stress Response
Oxidative Stress

Research Areas 2

Life sciences / Pharmacology /
Life sciences / Pharmaceuticals - health and biochemistry /

Awards 17

High Citation Award

2023/05　（SFRR-Japan）
Investigator Award

2021/03　(SFRR-International)
学術賞（日本酸化ストレス学会）

2018
International Prize (SFRR-International)

2018
学術奨励賞 ( 日本酸化ストレス学会 )

2012
Young Investigator Award ( SFRR-JAPAN )

2012
One of Elsevier's Top 10 Cited Articles on Scopus 2007-2008 in NeuroToxicology

2010
学術奨励賞 ( ビタミンE研究会 )

2009
学術奨励賞 ( 日本フリーラジカル学会 / 日本過酸化脂質フリーラジカル学会 )

2007
Young Investigator Award ( SFRR-Japan )

2007
Young Investigator Award ( SFRR-Asia )

2005
Travel Grant for Young Scientists ( International Interdisciplinary Conference on Vitamins, Coenzymes, and Biofactors 2005 )

2005
Young Investigator Award ( SFRR-Asia )

2005
Travel Grant for Young Scientists ( International Interdisciplinary Conference on Vitamins, Coenzymes, and Biofactors 2005 )

2005
Fellowship Award ( A New York Academy of Sciences Conference Vitamin E and Health )

2004
Fellowship Award ( A New York Academy of Sciences Conference Vitamin E and Health )

2004
Prize for Emcouragement (Antioxidant Biofactor Research Society)

2004

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Papers 180

Gender differences in plasma element concentrations and associations between selenoprotein P and iron metabolism in a community-based cohort study. International-journal

Yoshiro Saito, Misaki Shimizu, Mitsuharu Sato, An Masuda, Kotoko Arisawa, Keiko Taguchi, Takashi Toyama, Ikuko N Motoike, Kengo Kinoshita, Seizo Koshiba, Masayuki Yamamoto, Toshinari Takamura

Scientific reports　15　(1)　25319-25319　2025/07/13

DOI： 10.1038/s41598-025-10581-2 　

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Essential trace elements, such as iron (Fe) and selenium (Se), play physiological roles in our body, whereas environmental toxic metals, such as arsenic (As), cadmium (Cd), and mercury (Hg), are known to be associated with various disease risks. However, the relationship between elements, biochemical parameters, and lifestyle habits based on multi-elemental analysis in healthy individuals has not been fully verified. Multi-elemental analysis is useful for evaluating the change in the concentration of these elements and metals. In the present study using totally 100 µL plasma samples from the Tohoku Medical Megabank (TMM) community-based cohort study (total of 506 specimens), we conducted a multi-elemental analysis to evaluate 14 elements in generally healthy subjects. We further determined Se-transporter selenoprotein P levels using the originally developed ELISA method, since increases and decreases in selenoprotein P levels are associated with various disease risks. Multiple correlation analyses between the obtained measured values and several factors suggest that elements such as Fe, Se, and Hg, as well as selenoprotein P levels, are associated with gender differences. We also found that factors such as Fe, Se, As, Hg, hematocrit value, hemoglobin (Hb) content, and HbA1c are correlated with selenoprotein P levels. Furthermore, correlations between Fe levels and Hb content and between As/Hg and fish consumption were found. These findings demonstrate the suitability of multi-elemental analyses with limited plasma sample amounts, clearly show gender-differentiated elements, and establish a significant relationship between selenoprotein P and Fe metabolism.
Lactoferrin attenuates renal fibrosis and uremic sarcopenia in a mouse model of adenine-induced chronic kidney disease

Yukina Iwamoto, Seiko Yamakoshi, Akiyo Sekimoto, Koji Hosomi, Takashi Toyama, Yoshiro Saito, Jun Kunisawa, Nobuyuki Takahashi, Eikan Mishima, Emiko Sato

The Journal of Nutritional Biochemistry　2025/07

DOI： 10.1016/j.jnutbio.2025.110039 　
The selenoprotein P/ApoER2 axis facilitates selenium accumulation in selenoprotein P-accepting cells and confers prolonged resistance to ferroptosis. International-journal

Atsuya Ichikawa, Takashi Toyama, Hiroki Taguchi, Satoru Shiina, Hayato Takashima, Kazuaki Takahashi, Yasumitsu Ogra, Ayako Mizuno, Kotoko Arisawa, Yoshiro Saito

Redox biology　83　103664-103664　2025/06

DOI： 10.1016/j.redox.2025.103664 　

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The essential trace element selenium (Se) plays a significant role in redox homeostasis, while Se is very reactive and has a potent toxicity. Understanding the molecular machinery that supports Se metabolism is important for the both physiological and pathophysiological context. Incorporated Se is translated/transformed in the liver into selenoprotein P (SeP; encoded by Selenop), an extracellular Se carrier protein that effectively transports Se to the cells via the binding to its receptor apolipoprotein E receptor 2 (ApoER2), which is taken up by cells. The present study shows that SeP is a source of Se that accumulates intracellularly and can be utilized for prolonged periods under Se-deficient conditions. In cultured cells (RD and SH-SY5Y), glutathione peroxidase (GPX) expression induced by Se supply via the SeP/ApoER2 pathway was maintained longer during Se deficiency than inorganic Se, which was promoted by ApoER2 overexpression. SeP-deficient mice showed a faster decline in brain Se levels when fed a Se-deficient diet. Preserved GPX expression induced by this SeP/ApoER2 axis contributed to oxidative stress and ferroptosis resistance, suggesting that this redundant Se metabolism contributes to prolonged Se utilization and cytoprotection.
Lipid peroxidation, ferroptosis, and antioxidants. International-journal

Noriko Noguchi, Yoshiro Saito, Etsuo Niki

Free radical biology & medicine　237　228-238　2025/05/13

DOI： 10.1016/j.freeradbiomed.2025.05.393 　

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The discovery and conceptualization of ferroptosis as regulated, iron-catalyzed cell death driven by excessive lipid peroxidation triggered re-evaluation of lipid hydroperoxides in connection with health and disease. Free and ester forms of polyunsaturated fatty acids (PUFAs) are oxidized in vivo by multiple oxidizing species to produce lipid hydroperoxides as primary products, some purposely while others unintentionally. The detailed analysis of isomer distribution of lipid hydroperoxides enables us to identify the responsible oxidants. Linoleates, the most abundant PUFA in humans, are oxidized to give multiple isomers of hydroperoxyoctadecadienoates (H(p)ODEs) as primary major products, racemic trans, trans-9- and 13-H(p)ODEs, 13(S)-cis, trans-H(p)ODE, and 10- and 12-H(p)ODEs being specific biomarker for the oxidation by free radicals, lipoxygenase (LOX), and singlet oxygen, respectively. Cholesterol is another important lipid and its hydroperoxides are produced solely by non-enzymatic oxidation, the major products being cholesterol 7-hydroperoxide and 5-hydroperoxide by free radicals and singlet oxygen, respectively. The available data obtained from human samples show that lipid hydroperoxides are produced in vivo primarily by free radical mediated lipid peroxidation and that the contribution of LOXs and singlet oxygen is small. Multiple antioxidants having different functions play their respective roles in the physiological defense network against detrimental lipid peroxidation and ferroptosis. The fact that lipid hydroperoxides are produced in vivo mainly by free radical mediated lipid peroxidation suggests that radical scavenging antioxidants act as essential ferroptosis inhibitors, which was substantiated by many studies. Considering the reactivity and physiological concentrations, it may be said that vitamins E and C play the primary roles as biological radical scavenging antioxidants against ferroptosis by synergistic interactions. Novel synthetic antioxidants with higher reactivity than natural antioxidants have been reported and their biological effects should be assessed. The factors that determine antioxidant effects in vivo are critically reviewed.
Cysteine redoxome landscape in mouse brown adipose tissue under acute cold exposure. International-journal

Hein Ko Oo, Cynthia M Galicia-Medina, Takumi Nishiuchi, Ryota Tanida, Hisanori Goto, Yujiro Nakano, Yumie Takeshita, Yoshiro Saito, Hiroaki Takayama, Toshinari Takamura

iScience　28　(3)　112051-112051　2025/03/21

DOI： 10.1016/j.isci.2025.112051 　

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Reversible cysteine post-translational modifications serve as a "switch" for protein structure-function dynamics. While reversible cysteine oxidation in uncoupling protein 1 is known to play a role in brown fat thermogenesis, the full cysteine redoxome affected by cold exposure remains unexplored. We established a strategy for comprehensively mapping the cysteine redoxome by pinpointing oxidized and reduced cysteine residues in the brown adipose tissue of mice under room temperature and acute cold exposure. We identified over 1,000 labeled cysteine residues under room and cold temperatures. Cold exposure shifted the cysteine redox states toward oxidation. Cold-sensitive reactive cysteine residues were enriched in biological processes and molecular functions associated with thermogenesis pathways. The presence of proximal positively charged and negatively charged amino acids determined the highly reactive and non-reactive cysteine residues, respectively, under cold exposure. Our findings broaden the landscape of cold-sensitive proteome and identify potential therapeutic targets to fine-tune thermogenesis.
Assessing the role of selenium in Minamata disease through reanalysis of historical samples. International-journal

Mineshi Sakamoto, Masumi Marumoto, Koichi Haraguchi, Takashi Toyama, Yoshiro Saito, Steven J Balogh, Chiharu Tohyama, Masaaki Nakamura

Environment international　195　109242-109242　2025/01

DOI： 10.1016/j.envint.2024.109242 　

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Minamata disease, a severe neurological disorder identified in Japan in 1956, results from methylmercury (MeHg) intoxication in humans due to environmental contamination. Before MeHg was recognized as the cause, selenium (Se) was suspected of being the potential cause owing to elevated Se levels in patients' organs. Subsequent animal studies indicated that Se mitigates MeHg toxicity; however, its role in Minamata disease remains unexplored. We analyzed Hg and Se in historical samples of the industrial wastes (n = 4) on the factory site, sediments (n = 9), and fish/shellfish (n = 16) in Minamata Bay, and organs of patients with Minamata disease (n = 12). All samples showed elevated levels of both Hg and Se, providing the first evidence that Se was also discharged into Minamata Bay, entering the food chain and accumulating at high levels in patient organs. The Hg/Se molar ratio in contaminated shellfish (median > 3.0) indicated exceptionally high MeHg exposure, far exceeding the ordinary level (< 1.0). Patients exhibited significantly increased Se levels in the liver and kidney but lower amounts in the brain. Notably, median Hg/Se molar ratios exceeding 4.0 were observed, particularly in the cerebrum and cerebellum in acute cases, closely mirroring the molar ratios found in seafood. The elevated Hg/Se molar ratio in the brain helps explain the severe neurological damage in patients' central nervous systems, despite higher Hg levels in the liver and kidney compared to the brain. These findings provide important insight into the mechanism of MeHg intoxication and highlight the risks associated with MeHg-contaminated seafood, aiding efforts to protect consumers.
Conjugated fatty acids drive ferroptosis through chaperone-mediated autophagic degradation of GPX4 by targeting mitochondria. International-journal

Yusuke Hirata, Yuto Yamada, Soma Taguchi, Ryota Kojima, Haruka Masumoto, Shinnosuke Kimura, Takuya Niijima, Takashi Toyama, Ryoji Kise, Emiko Sato, Yasunori Uchida, Junya Ito, Kiyotaka Nakagawa, Tomohiko Taguchi, Asuka Inoue, Yoshiro Saito, Takuya Noguchi, Atsushi Matsuzawa

Cell death & disease　15　(12)　884-884　2024/12/06

DOI： 10.1038/s41419-024-07237-w 　

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Conjugated fatty acids (CFAs) have been known for their anti-tumor activity. However, the mechanism of action remains unclear. Here, we identify CFAs as inducers of glutathione peroxidase 4 (GPX4) degradation through chaperone-mediated autophagy (CMA). CFAs, such as (10E,12Z)-octadecadienoic acid and α-eleostearic acid (ESA), induced GPX4 degradation, generation of mitochondrial reactive oxygen species (ROS) and lipid peroxides, and ultimately ferroptosis in cancer cell lines, including HT1080 and A549 cells, which were suppressed by either pharmacological blockade of CMA or genetic deletion of LAMP2A, a crucial molecule for CMA. Mitochondrial ROS were sufficient and necessary for CMA-dependent GPX4 degradation. Oral administration of an ESA-rich oil attenuated xenograft tumor growth of wild-type, but not that of LAMP2A-deficient HT1080 cells, accompanied by increased lipid peroxidation, GPX4 degradation and cell death. Our study establishes mitochondria as the key target of CFAs to trigger lipid peroxidation and GPX4 degradation, providing insight into ferroptosis-based cancer therapy.
Modifications of DJ-1 in which pI shifts to acidic in red blood cells a potential biomarker for Parkinson's disease at early stages. International-journal

Kohei Matsuda, Yuichiro Mita, Kazumasa Saigoh, Yoshiro Saito, Noriko Noguchi

Free radical research　58　(11)　1-10　2024/11/22

DOI： 10.1080/10715762.2024.2430536 　

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Parkinson's disease (PD) is one of the most common neurodegenerative diseases, the incidence of which increases with age. However, since there is no fundamental treatment or methods for early diagnosis, new methods of treatment and diagnosis are urgently needed. We focused on post-translational modifications of DJ-1, which is encoded by the familial PD-causative gene PARK7 in red blood cells (RBCs). DJ-1 has three cysteines (Cys46, Cys53, and Cys106), with Cys106 being preferentially oxidized. We previously reported that sulfinated/sulfonated Cys106 DJ-1 (oxDJ-1) is increased in the RBCs of PD patients. In this study, we analyzed RBC-derived DJ-1 from PD patients and control subjects by 2-dimensional electrophoresis. We found that the ratio of the spot of DJ-1 with a more acidic isoelectric point than oxDJ-1 was increased more significantly than that of oxDJ-1 in RBCs from patients at the early stage of unmedicated PD and decreased with the progression of PD stage and treatment. Furthermore, we revealed that this acidic spot of DJ-1 increased upon exposure to H2O2. However, when either Cys53 or Cys106 of DJ-1 was replaced with serine, there was no significant increase in the acidic spot caused by H2O2. In this study, we propose a new biomarker for early diagnosis of PD using both the ratios of oxDJ-1 to total DJ-1 and the acidic spot of DJ-1 to total DJ-1.
Remodeling of Selenium Metabolism through Adduct Formation of Selenoprotein P with Epigallocatechin Gallate Peer-reviewed

Takashi Toyama, Katsuki Sato, Yoshiro Saito

Metallomics Research　4　(3)　1-6　2024/11

DOI： 10.11299/metallomicsresearch.MR202403 　
PRDX6 dictates ferroptosis sensitivity by directing cellular selenium utilization

Junya Ito, Toshitaka Nakamura, Takashi Toyama, Deng Chen, Carsten Berndt, Gereon Poschmann, André Santos Dias Mourão, Sebastian Doll, Mirai Suzuki, Weijia Zhang, Jiashuo Zheng, Dietrich Trümbach, Naoya Yamada, Koya Ono, Masana Yazaki, Yasutaka Kawai, Mieko Arisawa, Yusuke Ohsaki, Hitoshi Shirakawa, Adam Wahida, Bettina Proneth, Yoshiro Saito, Kiyotaka Nakagawa, Eikan Mishima, Marcus Conrad

Molecular Cell　2024/11
Publisher: Elsevier BV
DOI： 10.1016/j.molcel.2024.10.028 　

ISSN： 1097-2765
Inhibition of Selenium Supply Function of Selenoprotein P through Adduct Formation by Sulforaphane. International-journal

Xinying Ye, Takashi Toyama, Wang Yinuo, Runa Kudo, Siu Stephanie, Kotoko Arisawa, Yoshiro Saito

The Journal of nutritional biochemistry　135　109781-109781　2024/10/15

DOI： 10.1016/j.jnutbio.2024.109781 　

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Selenium is a potent nucleophile essential for selenoenzymes, such as glutathione peroxidase (also known as GSH-Px; GPX; GPx) and selenoprotein P (also known as SelP; SEPP1; SELENOP; SeP). SeP is predominantly secreted from the liver and functions as a selenium carrier in plasma. We previously found that sulforaphane, an electrophilic phytochemical, reduces SeP production in cultured hepatocytes and mouse liver, however, the effect of electrophilic modification of SeP by SFN on selenium transport and metabolism remains unclear. In the present study, we demonstrate that sulforaphane covalently modifies selenocysteine/cysteine residues of SeP using an acidic biotin PAEC5 maleimide labeling assay, which allows for focused-labeling of selenocysteine residues. Although the SFN-SeP adduct can be taken up by HepG2 cells and degraded by the lysosome, it was less effective in inducing GPx expression. Our findings indicate that SFN disrupts the selenium supply pathway through the formation of the SeP-SFN adduct.
Differential associations between selenoprotein P and distal sensorimotor polyneuropathy in people with and without diabetes: KORA F4/FF4 study International-journal

Christian Herder, Yoshiro Saito, Maria C. Spagnuolo, Haifa Maalmi, Misaki Shimizu, Gidon J. Bönhof, Keita Suzuki, Wolfgang Rathmann, Annette Peters, Michael Roden, Dan Ziegler, Barbara Thorand, Toshinari Takamura

Free Radical Biology and Medicine　223　87-95　2024/10
Publisher: Elsevier BV
DOI： 10.1016/j.freeradbiomed.2024.07.028 　

ISSN： 0891-5849

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BACKGROUND: Oxidative stress is a risk factor for distal sensorimotor polyneuropathy (DSPN). Selenoprotein P is a protein with antioxidant properties but has not been investigated in the context of DSPN. This study aimed to assess the associations between selenoprotein P and DSPN in people without and with type 2 diabetes (T2D). METHODS: Cross-sectional and prospective analyses were based on 1053 (including 217 with T2D) and 513 participants (including 79 with T2D), respectively, aged 61-82 years from the population-based KORA F4 survey. DSPN at baseline (KORA F4) and in the follow-up survey KORA FF4 was defined based on the Michigan Neuropathy Screening Instrument. Serum levels of full-length selenoprotein P were quantified by ELISA. Associations between selenoprotein P and prevalent or incident DSPN were estimated using logistic regression analysis adjusting for multiple confounders. RESULTS: Selenoprotein P levels were not associated with prevalent DSPN in the total sample. However, there was a significant interaction by diabetes status. Higher levels of selenoprotein P were associated with lower odds of prevalent DSPN in individuals without T2D (fully adjusted model: OR 0.825 [95 % CI 0.682, 0.998], p = 0.0476), but not in those with T2D (OR [95 % CI] 1.098 [0.829, 1.454], p = 0.5132; pinteraction = 0.0488). Selenoprotein P levels were not associated with incident DSPN over a follow-up of 6.5 years. CONCLUSION: In individuals without T2D from the older general population, lower selenoprotein P levels were associated with a higher prevalence of DSPN. Whether the antioxidant properties of selenoprotein P are responsible for the observed associations remains to be elucidated in future research.
Ferroptosis in health and disease. International-journal

Carsten Berndt, Hamed Alborzinia, Vera Skafar Amen, Scott Ayton, Uladzimir Barayeu, Alexander Bartelt, Hülya Bayir, Christina M Bebber, Kivanc Birsoy, Jan P Böttcher, Simone Brabletz, Thomas Brabletz, Ashley R Brown, Bernhard Brüne, Giorgia Bulli, Alix Bruneau, Quan Chen, Gina M DeNicola, Tobias P Dick, Ayelén Distéfano, Scott J Dixon, Jan B Engler, Julia Esser-von Bieren, Maria Fedorova, José Pedro Friedmann Angeli, Manuel A Friese, Dominic C Fuhrmann, Ana J García-Sáez, Karolina Garbowicz, Magdalena Götz, Wei Gu, Linda Hammerich, Behrouz Hassannia, Xuejun Jiang, Aicha Jeridi, Yun Pyo Kang, Valerian E Kagan, David B Konrad, Stefan Kotschi, Peng Lei, Marlène Le Tertre, Sima Lev, Deguang Liang, Andreas Linkermann, Carolin Lohr, Svenja Lorenz, Tom Luedde, Axel Methner, Bernhard Michalke, Anna V Milton, Junxia Min, Eikan Mishima, Sebastian Müller, Hozumi Motohashi, Martina U Muckenthaler, Shohei Murakami, James A Olzmann, Gabriela Pagnussat, Zijan Pan, Thales Papagiannakopoulos, Lohans Pedrera Puentes, Derek A Pratt, Bettina Proneth, Lukas Ramsauer, Raphael Rodriguez, Yoshiro Saito, Felix Schmidt, Carina Schmitt, Almut Schulze, Annemarie Schwab, Anna Schwantes, Mariluz Soula, Benedikt Spitzlberger, Brent R Stockwell, Leonie Thewes, Oliver Thorn-Seshold, Shinya Toyokuni, Wulf Tonnus, Andreas Trumpp, Peter Vandenabeele, Tom Vanden Berghe, Vivek Venkataramani, Felix C E Vogel, Silvia von Karstedt, Fudi Wang, Frank Westermann, Chantal Wientjens, Christoph Wilhelm, Michele Wölk, Katherine Wu, Xin Yang, Fan Yu, Yilong Zou, Marcus Conrad

Redox biology　75　103211-103211　2024/09

DOI： 10.1016/j.redox.2024.103211 　

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Ferroptosis is a pervasive non-apoptotic form of cell death highly relevant in various degenerative diseases and malignancies. The hallmark of ferroptosis is uncontrolled and overwhelming peroxidation of polyunsaturated fatty acids contained in membrane phospholipids, which eventually leads to rupture of the plasma membrane. Ferroptosis is unique in that it is essentially a spontaneous, uncatalyzed chemical process based on perturbed iron and redox homeostasis contributing to the cell death process, but that it is nonetheless modulated by many metabolic nodes that impinge on the cells' susceptibility to ferroptosis. Among the various nodes affecting ferroptosis sensitivity, several have emerged as promising candidates for pharmacological intervention, rendering ferroptosis-related proteins attractive targets for the treatment of numerous currently incurable diseases. Herein, the current members of a Germany-wide research consortium focusing on ferroptosis research, as well as key external experts in ferroptosis who have made seminal contributions to this rapidly growing and exciting field of research, have gathered to provide a comprehensive, state-of-the-art review on ferroptosis. Specific topics include: basic mechanisms, in vivo relevance, specialized methodologies, chemical and pharmacological tools, and the potential contribution of ferroptosis to disease etiopathology and progression. We hope that this article will not only provide established scientists and newcomers to the field with an overview of the multiple facets of ferroptosis, but also encourage additional efforts to characterize further molecular pathways modulating ferroptosis, with the ultimate goal to develop novel pharmacotherapies to tackle the various diseases associated with - or caused by - ferroptosis.
Endocytic vesicles act as vehicles for glucose uptake in response to growth factor stimulation International-journal

Ryouhei Tsutsumi, Beatrix Ueberheide, Feng-Xia Liang, Benjamin G. Neel, Ryuichi Sakai, Yoshiro Saito

Nature Communications　15　(1)　2843-2843　2024/04/02

DOI： 10.1038/s41467-024-46971-9 　

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Glycolysis is a fundamental cellular process, yet its regulatory mechanisms remain incompletely understood. Here, we show that a subset of glucose transporter 1 (GLUT1/SLC2A1) co-endocytoses with platelet-derived growth factor (PDGF) receptor (PDGFR) upon PDGF-stimulation. Furthermore, multiple glycolytic enzymes localize to these endocytosed PDGFR/GLUT1-containing vesicles adjacent to mitochondria. Contrary to current models, which emphasize the importance of glucose transporters on the cell surface, we find that PDGF-stimulated glucose uptake depends on receptor/transporter endocytosis. Our results suggest that growth factors generate glucose-loaded endocytic vesicles that deliver glucose to the glycolytic machinery in proximity to mitochondria, and argue for a new layer of regulation for glycolytic control governed by cellular membrane dynamics.
Cholesterol is more readily oxidized than phospholipid linoleates in cell membranes to produce cholesterol hydroperoxides

Yoshiro Saito, Noriko Noguchi, Etsuo Niki

Free Radical Biology and Medicine　2024/02

DOI： 10.1016/j.freeradbiomed.2023.12.011 　
Selenoprotein P expression in glioblastoma as a regulator of ferroptosis sensitivity: preservation of GPX4 via the cycling-selenium storage International-journal

Xi Zheng, Takashi Toyama, Stephanie Siu, Takayuki Kaneko, Hikari Sugiura, Shota Yamashita, Yoshiteru Shimoda, Masayuki Kanamori, Kotoko Arisawa, Hidenori Endo, Yoshiro Saito

Scientific Reports　14　(1)　682-682　2024/01/05
Publisher: Springer Science and Business Media LLC
DOI： 10.1038/s41598-024-51259-5 　

eISSN： 2045-2322

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Abstract Glioblastoma (GBM) is one of the most aggressive and deadly brain tumors; however, its current therapeutic strategies are limited. Selenoprotein P (SeP; SELENOP, encoded by the SELENOP gene) is a unique selenium-containing protein that exhibits high expression levels in astroglia. SeP is thought to be associated with ferroptosis sensitivity through the induction of glutathione peroxidase 4 (GPX4) via selenium supplementation. In this study, to elucidate the role of SeP in GBM, we analyzed its expression in GBM patients and found that SeP expression levels were significantly higher when compared to healthy subjects. Knock down of SeP in cultured GBM cells resulted in a decrease in GPX1 and GPX4 protein levels. Under the same conditions, cell death caused by RSL3, a ferroptosis inducer, was enhanced, however this enhancement was canceled by supplementation of selenite. These results indicate that SeP expression contributes to preserving GPX and selenium levels in an autocrine/paracrine manner, i.e., SeP regulates a dynamic cycling-selenium storage system in GBM. We also confirmed the role of SeP expression in ferroptosis sensitivity using patient-derived primary GBM cells. These findings indicate that expression of SeP in GBM can be a significant therapeutic target to overcome anticancer drug resistance.
Impact of selenium content in fetal bovine serum on ferroptosis susceptibility and selenoprotein expression in cultured cells.

Hayato Takashima, Takashi Toyama, Eikan Mishima, Kei Ishida, Yinuo Wang, Atsuya Ichikawa, Junya Ito, Syunsuke Yogiashi, Stephanie Siu, Mayumi Sugawara, Satoru Shiina, Kotoko Arisawa, Marcus Conrad, Yoshiro Saito

The Journal of toxicological sciences　49　(12)　555-563　2024

DOI： 10.2131/jts.49.555 　

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Ferroptosis, a mode of cell death involving iron-dependent lipid peroxidation, has attracted widespread attention in the development of anticancer drugs and toxicological studies as a potential mechanism of chemical-induced cytotoxicity. This process is regulated by several antioxidant enzymes, of which the selenium-containing glutathione peroxidase 4 (GPx4) is the prime regulator. However, accurately and reproducibly evaluating ferroptosis in cultured cells is challenging since numerous experimental factors in in vitro setting can influence the results. In the present study, we found that the expression levels of selenoproteins, such as GPx4 and GPx1, fluctuate across several cell lines depending on the selenium content of different origin of fetal bovine serum (FBS). Cells cultured in FBS containing higher selenium concentrations exhibited elevated GPx4 expression, and were resistant to ferroptosis induced by erastin and RSL3. These findings suggest that the variability of selenium content in different FBS batches can significantly influence the susceptibility of cells to ferroptosis, highlighting the importance of standardizing these factors to enhance the reproducibility of ferroptosis-related experiments.
Ccdc152 is not necessary for male fertility, but contributes to maintaining sperm morphology

Ryua HARIMA, Takahiro SASAKI, Takayuki KANEKO, Fuka ASO, Hayato TAKASHIMA, Takashi TOYAMA, Kenshiro HARA, Kentaro TANEMURA, Yoshiro SAITO

Journal of Reproduction and Development　70　(6)　396-404　2024
Publisher: Japanese Society of Animal Reproduction
DOI： 10.1262/jrd.2024-058 　

ISSN： 0916-8818

eISSN： 1348-4400

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Selenoprotein P (SeP) is synthesized in the liver and plays a vital role in maintaining selenium homeostasis via transport throughout the body. Previous studies have shown that SeP-deficient mice have severely reduced expression of selenoproteins essential for testicular function, leading to male infertility. We previously reported that the high expression of Ccdc152 in hepatocytes acts as a lncRNA, suppressing SeP expression in the liver. Ccdc152 reduces SeP translation by binding to SeP mRNA and decreasing its interaction with SECIS-binding protein 2. Although Ccdc152 is highly expressed in testes, its function remains unclear. Therefore, this study aimed to elucidate the role of Ccdc152 in the testes. Using the CRISPR/Cas9 system, we generated mice lacking all exons of Ccdc152 and found that SeP expression levels in the liver and plasma, as well as overall selenium homeostasis, remained unchanged. No significant differences were observed in the expression of glutathione peroxidase 1/4 or level of selenium in the testes. Subsequent investigation of the impact on male reproductive function revealed no abnormalities in sperm motility or Mendelian ratios of the offspring. However, a slight decrease in testicular weight and an increased rate of sperm malformations in the epididymis were observed. RNA-seq and pathway analyses identified the reduced expression of multiple genes related to kinesin and reproductive pathways. Based on these findings, Ccdc152 may not be essential for male reproductive function, but it may enhance reproductive capabilities by maintaining the expression of genes necessary for reproduction.
メチル水銀の解毒代謝におけるグルタチオンと超硫黄の異なる役割

Takashi Toyama, Runa Kudo, Yoshiro Saito

YAKUGAKU ZASSHI　144　(1)　41-45　2024/01/01
Publisher: Pharmaceutical Society of Japan
DOI： 10.1248/yakushi.23-00162-1 　

ISSN： 0031-6903

eISSN： 1347-5231
Sulforaphane decreases serum selenoprotein P levels through enhancement of lysosomal degradation independent of Nrf2

Xinying Ye, Takashi Toyama, Keiko Taguchi, Kotoko Arisawa, Takayuki Kaneko, Ryouhei Tsutsumi, Masayuki Yamamoto, Yoshiro Saito

Communications Biology　6　(1)　2023/10/19
Publisher: Springer Science and Business Media LLC
DOI： 10.1038/s42003-023-05449-y 　

eISSN： 2399-3642

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Abstract Selenoprotein P (SeP) is a major selenoprotein in serum predominantly produced in the liver. Excess SeP impairs insulin secretion from the pancreas and insulin sensitivity in skeletal muscle, thus inhibition of SeP could be a therapeutic strategy for type 2 diabetes. In this study, we examine the effect of sulforaphane (SFN), a phytochemical of broccoli sprouts and an Nrf2 activator, on SeP expression in vitro and in vivo. Treatment of HepG2 cells with SFN decreases inter- and intra-cellular SeP levels. SFN enhances lysosomal acidification and expression of V-ATPase, and inhibition of this process cancels the decrease of SeP by SFN. SFN activates Nrf2 in the cells, while Nrf2 siRNA does not affect the decrease of SeP by SFN or lysosomal acidification. These results indicate that SFN decreases SeP by enhancing lysosomal degradation, independent of Nrf2. Injection of SFN to mice results in induction of cathepsin and a decrease of SeP in serum. The findings from this study are expected to contribute to developing SeP inhibitors in the future, thereby contributing to treating and preventing diseases related to increased SeP.
An efficient selenium transport pathway of selenoprotein P utilizing a high-affinity ApoER2 receptor variant and being independent of selenocysteine lyase

Ayako Mizuno, Takashi Toyama, Atsuya Ichikawa, Naoko Sakai, Yuya Yoshioka, Yukina Nishito, Renya Toga, Hiroshi Amesaka, Takayuki Kaneko, Kotoko Arisawa, Ryouhei Tsutsumi, Yuichiro Mita, Shun-ichi Tanaka, Noriko Noguchi, Yoshiro Saito

Journal of Biological Chemistry　299　(8)　105009-105009　2023/07
Publisher: Elsevier BV
DOI： 10.1016/j.jbc.2023.105009 　

ISSN： 0021-9258
Selenoprotein P concentrations and risk of progression from mild cognitive impairment to dementia. International-journal

Marco Vinceti, Teresa Urbano, Annalisa Chiari, Tommaso Filippini, Lauren A Wise, Manuela Tondelli, Bernhard Michalke, Misaki Shimizu, Yoshiro Saito

Scientific reports　13　(1)　8792-8792　2023/05/31

DOI： 10.1038/s41598-023-36084-6 　

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There is a growing literature investigating the effects of selenium on the central nervous system and cognitive function. However, little is known about the role of selenoprotein P, the main selenium transporter, which can also have adverse biological effects. We conducted a prospective cohort study of individuals aged 42-81 years who received a clinical diagnosis of mild cognitive impairment. Using sandwich ELISA methods, we measured full-length selenoprotein P concentrations in serum and cerebrospinal fluid to assess the relation with dementia incidence during a median follow-up of 47.3 months. We used Cox proportional hazards regression and restricted cubic splines to model such relation. Of the 54 participants, 35 developed dementia during follow-up (including 26 cases of Alzheimer's dementia). Selenoprotein P concentrations in serum and cerebrospinal fluid were highly correlated, and in spline regression analyses they each showed a positive non-linear association with dementia risk, particularly after excluding dementia cases diagnosed within 24 months of follow-up. We also observed differences in association according to the dementia subtypes considered. Risk ratios of dementia peaked at 2-6 at the highest levels of selenoprotein P, when compared to its median level, also depending on matrix, analytical methodology and dementia subtype. Findings of this study, the first to assess selenoprotein P levels in the central nervous system in vivo and the first to use a prospective study design to evaluate associations with dementia, suggest that higher circulating concentrations of selenoprotein P, both in serum and cerebrospinal fluid, predict progression of MCI to dementia. However, further confirmation of these findings is required, given the limited statistical precision of the associations and the potential for residual confounding.
Actions of Thiols, Persulfides, and Polysulfides as Free Radical Scavenging Antioxidants. International-journal

Noriko Noguchi, Yoshiro Saito, Etsuo Niki

Antioxidants & redox signaling　2023/05/08

DOI： 10.1089/ars.2022.0191 　

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SIGNIFICANCE: The essential roles of thiol compounds as redox signaling mediator and protector have been established. Recently, the roles of persulifdes and polysulfides as mediator involved in numerous physiological processes have been revealed. RECENT ADVANCES: It became possible recently to detect and measure persulfides and polysulfides in human fluids and tissues and their physiological functions including cellular signaling and protection against oxidative stress have been reported but the underlying mechanisms and dynamics remain elusive. CRITICAL ISSUES: The physiological functions of thiol compounds have been studied focusing primarily on two-electron redox reactions. In contrast, the contribution of one-electron redox mechanism, that is, free radical mediated oxidation and antioxidation have received much less attention. Considering the important effects of free radical mediated oxidation of biological molecules on pathophysiology, the antioxidant functions of thiol compounds as free radical scavenger are challenging issues. FUTURE DIRECTIONS: The antioxidant actions and dynamics of thiols, hydropersulfides and hydropolysulfides as free radical scavenging antioxidant and physiological significance remain to be established.
Lipid peroxidation increases membrane tension, Piezo1 gating, and cation permeability to execute ferroptosis. International-journal

Yusuke Hirata, Ruiqi Cai, Allen Volchuk, Benjamin E Steinberg, Yoshiro Saito, Atsushi Matsuzawa, Sergio Grinstein, Spencer A Freeman

Current biology : CB　33　(7)　1282-1294　2023/04/10

DOI： 10.1016/j.cub.2023.02.060 　

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The ongoing metabolic and microbicidal pathways that support and protect cellular life generate potentially damaging reactive oxygen species (ROS). To counteract damage, cells express peroxidases, which are antioxidant enzymes that catalyze the reduction of oxidized biomolecules. Glutathione peroxidase 4 (GPX4) is the major hydroperoxidase specifically responsible for reducing lipid peroxides; this homeostatic mechanism is essential, and its inhibition causes a unique type of lytic cell death, ferroptosis. The mechanism(s) that lead to cell lysis in ferroptosis, however, are unclear. We report that the lipid peroxides formed during ferroptosis accumulate preferentially at the plasma membrane. Oxidation of surface membrane lipids increased tension on the plasma membrane and led to the activation of Piezo1 and TRP channels. Oxidized membranes thus became permeable to cations, ultimately leading to the gain of cellular Na+ and Ca2+ concomitant with loss of K+. These effects were reduced by deletion of Piezo1 and completely inhibited by blocking cation channel conductance with ruthenium red or 2-aminoethoxydiphenyl borate (2-APB). We also found that the oxidation of lipids depressed the activity of the Na+/K+-ATPase, exacerbating the dissipation of monovalent cation gradients. Preventing the changes in cation content attenuated ferroptosis. Altogether, our study establishes that increased membrane permeability to cations is a critical step in the execution of ferroptosis and identifies Piezo1, TRP channels, and the Na+/K+-ATPase as targets/effectors of this type of cell death.
Antioxidant action of persulfides and polysulfides against free radical-mediated lipid peroxidation

Takayuki Kaneko, Yuichiro Mita, Kanako Nozawa-Kumada, Masana Yazaki, Mieko Arisawa, Etsuo Niki, Noriko Noguchi, Yoshiro Saito

Free Radical Research　56　(9-10)　1-14　2023/01/11
Publisher: Informa UK Limited
DOI： 10.1080/10715762.2023.2165918 　

ISSN： 1071-5762

eISSN： 1029-2470
必須微量元素セレン研究の最前線—ダイナミクスと生理／病理的意義，重金属毒性に対する作用

有澤琴子, 外山喬士, 斎藤芳郎

ファルマシア　59　(3)　179-184　2023
Publisher: 公益社団法人日本薬学会
DOI： 10.14894/faruawpsj.59.3_179 　

ISSN： 0014-8601

eISSN： 2189-7026

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必須微量元素セレンは、肝臓で合成・分泌される血漿セレン含有タンパク質セレノプロテインＰ (SeP) を介して全身に輸送される。SePは受容体を介したセレン輸送に加え、重金属に対する生体防御作用を担う。一方、SePの発現異常が糖尿病発症にも関与することが明らかとなってきた。我々はSePを軸として，セレンダイナミクスの理解とその生理的・病理的意義、および重金属毒性に関する衛生薬学的意義の解明に取り組んでいる。本項では、SePの構造と機能に関して解説するとともに、我々の最近の取り組みについて紹介する。
Circulating selenoprotein P levels predict glucose-lowering and insulinotropic effects of metformin, but not alogliptin: A post-hoc analysis.

Yumie Takeshita, Takeo Tanaka, Hiroaki Takayama, Yuki Kita, Hisanori Goto, Yujiro Nakano, Yoshiro Saito, Toshinari Takamura

Journal of diabetes investigation　14　(2)　230-235　2022/12/07

DOI： 10.1111/jdi.13949 　

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AIMS/INTRODUCTION: Selenoprotein P (SeP; encoded by SEPP1 in humans) is a hepatokine that causes impaired insulin secretion and insulin resistance. Metformin downregulates SELENOP promoter activity through an adenosine monophosphate-activated kinase-forkhead box protein O3a pathway in hepatocytes. This study aimed to test our hypothesis that circulating SeP levels are associated with the glucose-lowering effect of metformin in humans. MATERIALS AND METHODS: A total of 84 participants with poorly controlled type 2 diabetes were randomly assigned to receive metformin (1,000 mg, twice daily) or a dipeptidyl peptidase-4 inhibitor, alogliptin (25 mg, once daily) for 12 weeks. We tested metformin and alogliptin on SeP levels and factors associated therewith as a post-hoc analysis. RESULTS: Both metformin and aloglipitin did not change the SeP levels. Although metformin significantly increased the insulin secretory index secretory units of islets in transplantation only in participants with higher baseline SeP (>3.87), both agents similarly reduced fasting plasma glucose and glycated hemoglobin. SeP levels at baseline were correlated negatively with changes in SeP (r = -0.484, P = 0.004) and fasting plasma glucose (r = -0.433, P = 0.011), and positively with changes in C-peptide immunoreactivity (r = 0.420, P = 0.017) and secretory units of islets in transplantation (r = 0.388, P = 0.028) in the metformin, but not alogliptin, group. CONCLUSIONS: Higher baseline levels of SeP significantly predicted metformin-mediated, but not alogliptin-mediated, glucose-lowering and insulinotropic effects. Serum SeP levels might be a novel biomarker for predicting the outcomes of metformin therapy, which might be helpful in tailoring diabetes medication.
Metal-binding properties of selenoprotein P—its relation to structure and function Peer-reviewed

Takashi Toyama, Takayuki Kaneko, Kotoko Arisawa, Yoshiro Saito

Metallomics Research　2　(3)　18-27　2022/12

DOI： 10.11299/metallomicsresearch.MR202209 　
Selenoprotein P Concentrations in the Cerebrospinal Fluid and Serum of Individuals Affected by Amyotrophic Lateral Sclerosis, Mild Cognitive Impairment and Alzheimer’s Dementia International-journal

Teresa Urbano, Marco Vinceti, JESSICA MANDRIOLI, Annalisa Chiari, Tommaso Filippini, Roberta Bedin, Manuela Tondelli, Cecilia Simonini, Giovanna Zamboni, Misaki Shimizu, Yoshiro Saito

International Journal of Molecular Sciences　23　(17)　2022/08

DOI： 10.3390/ijms23179865 　

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Selenoprotein P, a selenium-transporter protein, has been hypothesized to play a role in the etiology of neurodegenerative diseases such as amyotrophic lateral sclerosis (ALS) and Alzheimer's dementia (AD). However, data in humans are scarce and largely confined to autoptic samples. In this case-control study, we determined selenoprotein P concentrations in both the cerebrospinal fluid (CSF) and the serum of 50 individuals diagnosed with ALS, 30 with AD, 54 with mild cognitive impairment (MCI) and of 30 controls, using sandwich enzyme-linked immunosorbent assay (ELISA) methods. We found a positive and generally linear association between CSF and serum selenoprotein P concentrations in all groups. CSF selenoprotein P and biomarkers of neurodegeneration were positively associated in AD, while for MCI, we found an inverted-U-shaped relation. CSF selenoprotein P concentrations were higher in AD and MCI than in ALS and controls, while in serum, the highest concentrations were found in MCI and ALS. Logistic and cubic spline regression analyses showed an inverse association between CSF selenoprotein P levels and ALS risk, and a positive association for AD risk, while an inverted-U-shaped relation with MCI risk emerged. Conversely, serum selenoprotein P concentrations were positively associated with risk of all conditions but only in their lower range. Overall, these findings indicate some abnormalities of selenoprotein P concentrations in both the central nervous system and blood associated with ALS and neurocognitive disorders, though in different directions. These alterations may reflect either phenomena of etiologic relevance or disease-induced alterations of nutritional and metabolic status.
Safety of selenium exposure and limitations of selenoprotein maximization: Molecular and epidemiologic perspectives International-journal

Marco Vinceti, Tommaso Filippini, Ewa Jablonska, Yoshiro Saito, Lauren A. Wise

Environmental Research　211　113092-113092　2022/08
Publisher: Elsevier {BV}
DOI： 10.1016/j.envres.2022.113092 　

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Recent evidence from laboratory and epidemiologic studies has shed a different light on selenium health effects and its recommended range of environmental exposure, compared with earlier research. Specifically, epidemiologic studies in Western populations have shown adverse effects of selenium exposure at low levels, sometimes below or slightly above selenium intakes needed to maximize selenoprotein expression and activity. In addition, three recent lines of evidence in molecular and biochemical studies suggest some potential drawbacks associated with selenoprotein maximization: 1) the possibility that selenoprotein upregulation is a compensatory response to oxidative challenge, induced by selenium itself or other oxidants; 2) the capacity of selenoproteins to trigger tumor growth in some circumstances; and 3) the deleterious metabolic effects of selenoproteins and particularly of selenoprotein P. The last observation provides a toxicological basis to explain why in humans selenium intake levels as low as 60 μg/day, still in the range of selenium exposure upregulating selenoprotein expression, might start to increase risk of type 2 diabetes. Overall, these new pieces of evidence from the literature call into question the purported benefit of selenoprotein maximization, and indicate the need to reassess selenium dietary reference values and upper intake level. This reassessment should clarify which range of selenoprotein upregulation follows restoration of adequate selenium availability and which range is driven by a compensatory response to selenium toxicity and oxidative stress.
Redox-sensitive DJ-1 protein: an insight into physiological roles, secretion, and therapeutic target

Biplab Kumar Dash, Yasuomi Urano, Yoshiro Saito, Noriko Noguchi

Redox Experimental Medicine　2022/07/01

DOI： 10.1530/REM-22-0007 　
Essential trace element selenium and redox regulation: its metabolism, physiological function, and related diseases

Yoshiro Saito

Redox Experimental Medicine　2022/07/01

DOI： 10.1530/REM-22-0010 　
Nephronectin influences EAE development by regulating the Th17/Treg balance via reactive oxygen species. International-journal

Machiko Honda, Tatsuya Segawa, Kiyoshi Ishikawa, Masahiro Maeda, Yoshiro Saito, Shigeyuki Kon

American journal of physiology. Cell physiology　322　(4)　C699-C711-C711　2022/04/01
Publisher: American Physiological Society
DOI： 10.1152/ajpcell.00376.2021 　

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Blood levels of the extracellular matrix protein nephronectin (Npnt), a protein critical for kidney development, are elevated in autoimmune experimental autoimmune encephalitis (EAE) mice, which are a model for multiple sclerosis. We found here that treatment with anti-Npnt antibody directed against the α8β1 integrin-binding site (Npnt-blocking antibody) inhibits EAE development. The selenium transporter selenoprotein P (SeP) was identified as a novel Npnt-binding partner. In EAE, Npnt induced SeP and glutathione peroxidase 1 (GPx1) expression, followed by reactive oxygen species (ROS) inhibition in CD4+ T cells; these changes were disturbed by Npnt-blocking antibody treatment, which also caused suppressed differentiation of interleukin (IL)-17-producing CD4+ T-helper cells (Th17s) and elevated differentiation of regulatory T cells (Tregs). Treatment of EAE mice with the ROS scavenger N-acetyl cysteine (NAC) blocked the Npnt-blocking antibody-induced decrease in Th17 differentiation and increase in Treg differentiation. In conclusion, the interaction between Npnt and SeP contributes to EAE development by regulating the Th17/Treg balance via the ROS level.
Role of selenoprotein P expression in the function of pancreatic β cells: Prevention of ferroptosis-like cell death and stress-induced nascent granule degradation International-journal

Nanako Kitabayashi, Shohei Nakao, Yuichiro Mita, Kotoko Arisawa, Takayuki Hoshi, Takashi Toyama, Kiyo-aki Ishii, Toshinari Takamura, Noriko Noguchi, Yoshiro Saito

Free Radical Biology and Medicine　183　89-103　2022/04
Publisher: Elsevier BV
DOI： 10.1016/j.freeradbiomed.2022.03.009 　

ISSN： 0891-5849

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Selenoprotein P (SELENOP) is a major selenium (Se)-containing protein (selenoprotein) in human plasma that is mainly synthesized in the liver. SELENOP transports Se to the cells, while SELENOP synthesized in peripheral tissues is incorporated in a paracrine/autocrine manner to maintain the levels of cellular selenoproteins, called the SELENOP cycle. Pancreatic β cells, responsible for the synthesis and secretion of insulin, are known to express SELENOP. Here, using MIN6 cells as a mouse model for pancreatic β cells and Selenop small interfering (si)RNA, we found that Selenop gene knockdown (KD) resulted in decreased cell viability, cellular pro/insulin levels, insulin secretion, and levels of several cellular selenoproteins, including glutathione peroxidase 4 (Gpx4) and selenoprotein K (Selenok). These dysfunctions induced by Selenop siRNA were recovered by the addition of Se. Ferroptosis-like cell death, regulated by Gpx4, was involved in the decrease of cell viability by Selenop KD, while stress-induced nascent granule degradation (SINGD), regulated by Selenok, was responsible for the decrease in proinsulin. SINGD was also observed in the pancreatic β cells of Selenop knockout mice. These findings indicate a significant role of SELENOP expression for the function of pancreatic β cells by maintaining the levels of cellular selenoproteins such as GPX4 and SELENOK.
Selenoprotein P-mediated reductive stress impairs cold-induced thermogenesis in brown fat. International-journal

Swe Mar Oo, Hein Ko Oo, Hiroaki Takayama, Kiyo-Aki Ishii, Yumie Takeshita, Hisanori Goto, Yujiro Nakano, Susumu Kohno, Chiaki Takahashi, Hiroyuki Nakamura, Yoshiro Saito, Mami Matsushita, Yuko Okamatsu-Ogura, Masayuki Saito, Toshinari Takamura

Cell reports　38　(13)　110566-110566　2022/03/29

DOI： 10.1016/j.celrep.2022.110566 　

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Reactive oxygen species (ROS) activate uncoupler protein 1 (UCP1) in brown adipose tissue (BAT) under physiological cold exposure and noradrenaline (NA) stimulation to increase thermogenesis. However, the endogenous regulator of ROS in activated BAT and its role in pathological conditions remain unclear. We show that serum levels of selenoprotein P (SeP; encoded by SELENOP) negatively correlate with BAT activity in humans. Physiological cold exposure downregulates Selenop in BAT. Selenop knockout mice show higher rectal temperatures and UCP1 sulfenylation during cold exposure. SeP treatment to brown adipocytes eliminated the NA-induced mitochondrial ROS by upregulating glutathione peroxidase 4 and impaired cellular thermogenesis. A high-fat/high-sucrose diet elevates serum SeP levels and diminishes the elevated NA-induced thermogenesis in BAT-Selenop KO mice. Therefore, SeP is the intrinsic factor inducing reductive stress that impairs thermogenesis in BAT and may be a potential therapeutic target for obesity and diabetes.
A non-nucleotide agonist that binds covalently to cysteine residues of STING Peer-reviewed

Kentaro Matsumoto, Shenwei Ni, Hiroyuki Arai, Takashi Toyama, Yoshiro Saito, Takehiro Suzuki, Naoshi Dohmae, Kojiro Mukai, Tomohiko Taguchi

Cell Structure and Function　48　(1)　59-70　2022
Publisher: Japan Society for Cell Biology
DOI： 10.1247/csf.22085 　

ISSN： 0386-7196

eISSN： 1347-3700
Effects of the Interplay between Selenocystine and Methylmercury on Their Cytotoxicity and Glucose-Driven Insulin Secretion from Mouse Insulinoma Cells

Daichi Chida, Takashi Toyama, Takanori Chiba, Takayuki Kaneko, Kotoko Arisawa, Yoshiro Saito

BPB Reports　5　(4)　74-79　2022
Publisher: Pharmaceutical Society of Japan
DOI： 10.1248/bpbreports.5.4_74 　

eISSN： 2434-432X
Methylmercury induces neuronal cell death by inducing TNF-α expression through the ASK1/p38 signaling pathway in microglia

Takashi Toyama, Takayuki Hoshi, Takuya Noguchi, Yoshiro Saito, Atsushi Matsuzawa, Akira Naganuma, Gi-Wook Hwang

Scientific Reports　11　(1)　2021/12

DOI： 10.1038/s41598-021-89210-7 　

eISSN： 2045-2322
Diverse cytoprotective actions of vitamin E isoforms- role as peroxyl radical scavengers and complementary functions with selenoproteins. International-journal

Yoshiro Saito

Free radical biology & medicine　175　121-129　2021/11/01
Publisher: Elsevier {BV}
DOI： 10.1016/j.freeradbiomed.2021.08.234 　

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Vitamin E, a generic term for tocopherol (T) and tocotrienol (T3), is one of the most potent lipid-soluble antioxidants in the body. It is classified into T and T3 based on the difference in the side chain structure. T and T3 have four isoforms: α-, β-, γ-, and δ, which have different chroman rings. Both T and T3 exhibit a similar ability to scavenge free radicals, and the extent of this ability depends on the difference in the chroman structure. However, they display unique cytoprotective activities in cultured cells depending on the difference in the side chain structure. The cytoprotective effects of vitamin E have received much attention in the prevention of ferroptosis, which is a distinct form of cell death involving iron-dependent lipid peroxidation. This review focuses on the cytoprotective actions of vitamin E isoforms against oxidative stress, particularly the difference between T and T3 and its relation to cellular uptake and distribution. Moreover, the molecular mechanism for cytoprotection of vitamin E oxidation products is explained, and the complementary role of vitamin E and selenoproteins to prevent lipid peroxidation and ferroptosis is described. Furthermore, the evaluation of vitamin E's radical scavenging activity in vivo using oxidative stress markers is discussed, particularly based on kinetic data and the physiological molar ratio of vitamin E to substrates, and the limited role of vitamin E as a peroxyl radical scavenger is described. The future directions and unresolved issues related to vitamin E and lipid peroxidation are also discussed.
Identification of a novel endogenous long non-coding RNA that inhibits selenoprotein P translation

Yuichiro Mita, Risa Uchida, Sayuri Yasuhara, Kohei Kishi, Takayuki Hoshi, Yoshitaka Matsuo, Tadashi Yokooji, Yoshino Shirakawa, Takashi Toyama, Yasuomi Urano, Toshifumi Inada, Noriko Noguchi, Yoshiro Saito

Nucleic Acids Research　2021/06/18
Publisher: Oxford University Press (OUP)
DOI： 10.1093/nar/gkab498 　

ISSN： 0305-1048

eISSN： 1362-4962

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<title>Abstract</title> Selenoprotein P (SELENOP) is a major plasma selenoprotein that contains 10 Sec residues, which is encoded by the UGA stop codon. The mRNA for SELENOP has the unique property of containing two Sec insertion sequence (SECIS) elements, which is located in the 3′ untranslated region (3′UTR). Here, we coincidentally identified a novel gene, CCDC152, by sequence analysis. This gene was located in the antisense region of the SELENOP gene, including the 3′UTR region in the genome. We demonstrated that this novel gene functioned as a long non-coding RNA (lncRNA) that decreased SELENOP protein levels via translational rather than transcriptional, regulation. We found that the CCDC152 RNA interacted specifically and directly with the SELENOP mRNA and inhibited its binding to the SECIS-binding protein 2, resulting in the decrease of ribosome binding. We termed this novel gene product lncRNA inhibitor of SELENOP translation (L-IST). Finally, we found that epigallocatechin gallate upregulated L-IST in vitro and in vivo, to suppress SELENOP protein levels. Here, we provide a new regulatory mechanism of SELENOP translation by an endogenous long antisense ncRNA.
Lipid peroxidation products as a mediator of toxicity and adaptive response - The regulatory role of selenoprotein and vitamin E. International-journal

Yoshiro Saito

Archives of biochemistry and biophysics　703　108840-108840　2021/05/30

DOI： 10.1016/j.abb.2021.108840 　

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Lipid peroxidation and its products have been investigated extensively and their biological importance, particularly in relation to physiological and pathophysiological conditions, has received considerable attention. Lipids are oxidized by three distinct mechanisms, i.e., enzymatic oxidation, nonenzymatic, free radical-mediated oxidation, and nonenzymatic, nonradical-mediated oxidation, which respectively yield specific products. Lipid hydroperoxides are the major primary products formed and are reduced to the corresponding hydroxides by antioxidative enzymes such as selenoproteins, and/or undergo secondary oxidation, generating various products with electrophilic properties, such as 4-hydroxy-2-nonenal. Lipid peroxidation induces a loss of fine structure and natural function of lipids, and can produce cytotoxicity and/or novel biological activity. This review broadly discusses the mechanisms of lipid peroxidation and its products, its utility as a biomarker for oxidative stress, the biological effects of lipid peroxidation products, including their action as a mediator of the adaptive response, and the role of the antioxidant system, particularly selenoproteins and vitamin E, in preventing lipid peroxidation and ferroptosis.
Identification of an endogenous long non-coding RNA that inhibits selenoprotein P translation- New regulatory mechanism of SeP translation

Yoshiro Saito

Free Radical Biology and Medicine　2021

DOI： 10.1016/J.FREERADBIOMED.2020.12.293 　
Selenium Transport Mechanism via Selenoprotein P-Its Physiological Role and Related Diseases. International-journal

Yoshiro Saito

Frontiers in nutrition　8　685517-685517　2021

DOI： 10.3389/fnut.2021.685517 　
Point mutation bias in SARS-CoV-2 variants results in increased ability to stimulate inflammatory responses. International-journal

Masato Kosuge, Emi Furusawa-Nishii, Koyu Ito, Yoshiro Saito, Kouetsu Ogasawara

Scientific reports　10　(1)　17766-17766　2020/10/20

DOI： 10.1038/s41598-020-74843-x 　

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Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection induces severe pneumonia and is the cause of a worldwide pandemic. Coronaviruses, including SARS-CoV-2, have RNA proofreading enzymes in their genomes, resulting in fewer gene mutations than other RNA viruses. Nevertheless, variants of SARS-CoV-2 exist and may induce different symptoms; however, the factors and the impacts of these mutations are not well understood. We found that there is a bias to the mutations occurring in SARS-CoV-2 variants, with disproportionate mutation to uracil (U). These point mutations to U are mainly derived from cytosine (C), which is consistent with the substrate specificity of host RNA editing enzymes, APOBECs. We also found the point mutations which are consistent with other RNA editing enzymes, ADARs. For the C-to-U mutations, the context of the upstream uracil and downstream guanine from mutated position was found to be most prevalent. Further, the degree of increase of U in SARS-CoV-2 variants correlates with enhanced production of cytokines, such as TNF-α and IL-6, in cell lines when compared with stimulation by the ssRNA sequence of the isolated virus in Wuhan. Therefore, RNA editing is a factor for mutation bias in SARS-CoV-2 variants, which affects host inflammatory cytokines production.
Hydrogen Peroxide Causes Cell Death via Increased Transcription of HOXB13 in Human Lung Epithelial A549 Cells. International-journal

Naoki Endo, Takashi Toyama, Akira Naganuma, Yoshiro Saito, Gi-Wook Hwang

Toxics　8　(4)　2020/09/28

DOI： 10.3390/toxics8040078 　

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Although homeobox protein B13 (HOXB13) is an oncogenic transcription factor, its role in stress response has rarely been examined. We previously reported that knockdown of HOXB13 reduces the cytotoxicity caused by various oxidative stress inducers. Here, we studied the role of HOXB13 in cytotoxicity caused by hydrogen peroxide in human lung epithelial A549 cells. The knockdown of HOXB13 reduced hydrogen peroxide-induced cytotoxicity; however, this phenomenon was largely absent in the presence of antioxidants (Trolox or N-acetyl cysteine (NAC)). This suggests that HOXB13 may be involved in the cytotoxicity caused by hydrogen peroxide via the production of reactive oxygen species (ROS). Hydrogen peroxide also increased both the mRNA and protein levels of HOXB13. However, these increases were rarely observed in the presence of a transcriptional inhibitor, which suggests that hydrogen peroxide increases protein levels via increased transcription of HOXB13. Furthermore, cell death occurred in A549 cells that highly expressed HOXB13. However, this cell death was mostly inhibited by treatment with antioxidants. Taken together, our findings indicate that HOXB13 may be a novel factor involved in the induction of oxidative stress, which causes cell death via intracellular ROS production.
The Association Between Concurrence of Infection and the Onset of Severe Eruption or Liver Injury in Patients Using Antipyretic Analgesics: A Matched, Nested Case‐Control Study

Takuya Imatoh, Kimie Sai, Yoshiro Saito

The Journal of Clinical Pharmacology　2020/09

DOI： 10.1002/jcph.1613 　
DJ-1-binding compound B enhances Nrf2 activity through the PI3-kinase-Akt pathway by DJ-1-dependent inactivation of PTEN. International-journal

Takeshi Niki, Jinro Endo, Kazuko Takahashi-Niki, Tatsuki Yasuda, Asami Okamoto, Yoshiro Saito, Hiroyoshi Ariga, Sanae M M Iguchi-Ariga

Brain research　1729　146641-146641　2020/02/15
Publisher: Elsevier {BV}
DOI： 10.1016/j.brainres.2019.146641 　

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DJ-1 was identified as an oncogene and also as a causative gene for a familial form of Parkinson disease (PD). DJ-1 plays various roles in anti-oxidative stress response. Superfluous oxidation of DJ-1 at cysteine residue 106 (C106), an inactive form of DJ-1, was observed in PD patients. DJ-1-binding compound B, which specifically bound to the C106 region of DJ-1, has been isolated and it has been shown to prevent oxidative stress-induced cell death through maintaining active forms of DJ-1 by inhibiting its superfluous oxidation. The molecular mechanism of the action of compound B, however, has not been fully elucidated. In this study, we found that compound B stimulated transcriptional activity of Nrf2 in H2O2-treated SH-SY5Y cells by inhibiting its degradation through the ubiquitin-proteasome system. Although Keap 1 is a major negative regulator of Nrf2, compound B strongly increased Nrf2 activity in Keap1-mutant A549 cells but not in PTEN-null PC3 and PTEN-knockout SH-SY5Y cells. Furthermore, treatment of cells with inhibitors of the PI3-kinase/Akt pathway inhibited the effect of compound B, and compound B increased the binding of PTEN to DJ-1 and decreased lipid phosphatase activity of PTEN concomitantly with increased oxidation of PTEN, an inactive form of PTEN. These results suggest that compound B enhances transcriptional activity of Nrf2 under an oxidative stress condition in a Keap1-independent manner and that its activity is elicited by activation of the PI3Kinase/Akt pathway with DJ-1-dependent inactivation of PTEN, leading to protection of oxidative stress-induced cell death.
Selenoprotein P as an in vivo redox regulator: disorders related to its deficiency and excess.

Yoshiro Saito

Journal of clinical biochemistry and nutrition　66　(1)　1-7　2020/01

DOI： 10.3164/jcbn.19-31 　
Selenoprotein P; P for Plasma, Prognosis, Prophylaxis, and More.

Ryouhei Tsutsumi, Yoshiro Saito

Biological & pharmaceutical bulletin　43　(3)　366-374　2020

DOI： 10.1248/bpb.b19-00837 　
Diagnostic and Prognostic Significance of Serum Levels of SeP (Selenoprotein P) in Patients With Pulmonary Hypertension. International-journal Peer-reviewed

Nobuhiro Kikuchi, Kimio Satoh, Taijyu Satoh, Nobuhiro Yaoita, Mohammad Abdul Hai Siddique, Junichi Omura, Ryo Kurosawa, Masamichi Nogi, Shinichiro Sunamura, Satoshi Miyata, Hirofumi Misu, Yoshiro Saito, Hiroaki Shimokawa

Arteriosclerosis, thrombosis, and vascular biology　39　(12)　2553-2562　2019/12

DOI： 10.1161/ATVBAHA.119.313267 　

ISSN： 1079-5642
Selenoprotein P as a significant regulator of pancreatic β cell function Peer-reviewed

Yoshiro Saito

The Journal of Biochemistry　2019/08/22
Publisher: Oxford University Press ({OUP})
DOI： 10.1093/jb/mvz061 　

ISSN： 0021-924X
Polymerization of Oxidized DJ-1 via Noncovalent and Covalent Binding: Significance of Disulfide Bond Formation Peer-reviewed

Mayuka Kobayashi, Kana Muramatsu, Takamitsu Haruyama, Haruka Uesugi, Ai Kikuchi, Hiroki Konno, Noriko Noguchi, Yoshiro Saito

ACS Omega　4　(6)　9603-9614　2019/06/30
Publisher: American Chemical Society ({ACS})
DOI： 10.1021/acsomega.9b00324 　
Circulating Concentrations of Insulin Resistance-Associated Hepatokines, Selenoprotein P and Leukocyte Cell-Derived Chemotaxin 2, during an Oral Glucose Tolerance Test in Humans. Peer-reviewed

Mohri K, Misu H, Takayama H, Ishii KA, Kikuchi A, Lan F, Enyama Y, Takeshita Y, Saito Y, Kaneko S, Takamura T

Biological & pharmaceutical bulletin　42　(3)　373-378　2019/03

DOI： 10.1248/bpb.b18-00549 　

ISSN： 0918-6158

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A hepatokine is a collective term for liver-derived secretory factors whose previously-unrecognized functions have been recently elucidated. We have rediscovered selenoprotein P (SeP) and leukocyte cell-derived chemotaxin 2 (LECT2) as hepatokines that are involved in the development of insulin resistance and hyperglycemia. The aim of this study was to determine whether and, if so, how oral glucose loading alters the two hepatokines in humans. We measured concentrations of serum SeP and plasma LECT2 during 75 g oral glucose tolerance test (OGTT) (n = 20) in people with various degrees of glucose tolerance. In OGTT, concentrations of both serum SeP and plasma LECT2 decreased at 120 min compared with the baseline values, irrespective of the severity of glucose intolerance. Decrement of serum SeP during OGTT showed no correlations to the clinical parameters associated with insulin resistance or insulin secretion. In multiple stepwise regression analyses, plasma cortisol was selected as the variable to explain the changes in plasma concentrations of LECT2. The current data reveal the acute inhibitory actions of oral intake of glucose on circulating SeP and LECT2 in humans, irrespective of the severity of glucose intolerance. This study suggests that circulating SeP is regulated by the unknown clinical factors other than insulin and glucose during OGTT.
Diagnostic and prognostic significance of serum levels of selenoprotein P in patients with pulmonary arterial hypertension

Yoshiro Saito

European Heart Journal　2019
Chemical Reactivity and Cellular Uptake of Tocopherols and Tocotrienols

Yoshiro Saito

Food Biosensors　2019
セレノプロテインPを用いた肺動脈性肺高血圧症の診断と予後評価法の開発 Peer-reviewed

菊地順裕, 佐藤公雄, 大村淳一, 佐藤大樹, 黒澤亮, 野木正道, 砂村慎一郎, 矢尾板信裕, 宮田敏, 御簾博文, 斎藤芳郎, 下川宏明

血管　42　(1)　54-54　2019/01
Publisher: 日本心脈管作動物質学会
ISSN： 0911-4637
Response by Kikuchi et al Regarding Article, "Selenoprotein P Promotes the Development of Pulmonary Arterial Hypertension: A Possible Novel Therapeutic Target". International-journal Peer-reviewed

Kikuchi N, Satoh K, Saito Y, Shimokawa H

Circulation　139　(5)　724-725　2019/01

DOI： 10.1161/CIRCULATIONAHA.118.038479 　

ISSN： 0009-7322
Serum selenoprotein P, but not selenium, predicts future hyperglycemia in a general Japanese population Peer-reviewed

Swe Mar Oo, Hirofumi Misu, Yoshiro Saito, Mutsumi Tanaka, Seiji Kato, Yuki Kita, Hiroaki Takayama, Yumie Takeshita, Takehiro Kanamori, Toru Nagano, Masatoshi Nakagen, Takeshi Urabe, Naoto Matsuyama, Shuichi Kaneko, Toshinari Takamura

Scientific Reports　8　(1)　16727　2018/12
Publisher: Springer Science and Business Media {LLC}
DOI： 10.1038/s41598-018-35067-2 　

eISSN： 2045-2322
Distribution of oxidized DJ-1 in Parkinson’s disease-related sites in the brain and in the peripheral tissues: effects of aging and a neurotoxin Peer-reviewed

Mita, Y., Kataoka, Y., Saito, Y., Kashi, T., Hayashi, K., Iwasaki, A., Imanishi, T., Miyasaka, T., Noguchi, N.

Scientific Reports　8　(1)　12056　2018/08/13
Publisher: Springer Nature
DOI： 10.1038/s41598-018-30561-z 　
Selenoprotein P Promotes the Development of Pulmonary Arterial Hypertension: Possible Novel Therapeutic Target. International-journal Peer-reviewed

Nobuhiro Kikuchi, Kimio Satoh, Ryo Kurosawa, Nobuhiro Yaoita, Md Elias-Al-Mamun, Mohammad Abdul Hai Siddique, Junichi Omura, Taijyu Satoh, Masamichi Nogi, Shinichiro Sunamura, Satoshi Miyata, Yoshiro Saito, Yasushi Hoshikawa, Yoshinori Okada, Hiroaki Shimokawa

Circulation　138　(6)　600-623　2018/08/07

DOI： 10.1161/CIRCULATIONAHA.117.033113 　

ISSN： 0009-7322

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BACKGROUND: Excessive proliferation and apoptosis resistance of pulmonary artery smooth muscle cells (PASMCs) are key mechanisms of pulmonary arterial hypertension (PAH). Despite the multiple combination therapy, a considerable number of patients develop severe pulmonary hypertension (PH) because of the lack of diagnostic biomarker and antiproliferative therapies for PASMCs. METHODS: Microarray analyses were used to identify a novel therapeutic target for PAH. In vitro experiments, including lung and serum samples from patients with PAH, cultured PAH-PASMCs, and high-throughput screening of 3336 low-molecular-weight compounds, were used for mechanistic study and exploring a novel therapeutic agent. Five genetically modified mouse strains, including PASMC-specific selenoprotein P (SeP) knockout mice and PH model rats, were used to study the role of SeP and therapeutic capacity of the compounds for the development of PH in vivo. RESULTS: Microarray analysis revealed a 32-fold increase in SeP in PAH-PASMCs compared with control PASMCs. SeP is a widely expressed extracellular protein maintaining cellular metabolism. Immunoreactivity of SeP was enhanced in the thickened media of pulmonary arteries in PAH. Serum SeP levels were also elevated in patients with PH compared with controls, and high serum SeP predicted poor outcome. SeP-knockout mice ( SeP-/-) exposed to chronic hypoxia showed significantly reduced right ventricular systolic pressure, right ventricular hypertrophy, and pulmonary artery remodeling compared with controls. In contrast, systemic SeP-overexpressing mice showed exacerbation of hypoxia-induced PH. Furthermore, PASMC-specific SeP-/- mice showed reduced hypoxia-induced PH compared with controls, whereas neither liver-specific SeP knockout nor liver-specific SeP-overexpressing mice showed significant differences with controls. Altogether, protein levels of SeP in the lungs were associated with the development of PH. Mechanistic experiments demonstrated that SeP promotes PASMC proliferation and resistance to apoptosis through increased oxidative stress and mitochondrial dysfunction, which were associated with activated hypoxia-inducible factor-1α and dysregulated glutathione metabolism. It is important to note that the high-throughput screening of 3336 compounds identified that sanguinarine, a plant alkaloid with antiproliferative effects, reduced SeP expression and proliferation in PASMCs and ameliorated PH in mice and rats. CONCLUSIONS: These results indicate that SeP promotes the development of PH, suggesting that it is a novel biomarker and therapeutic target of the disorder.
Diagnosis of Parkinson's disease and the level of oxidized DJ-1 protein. International-journal Peer-reviewed

Yuko Yamagishi, Kazumasa Saigoh, Yoshiro Saito, Ikuko Ogawa, Yoshiyuki Mitsui, Yukihiro Hamada, Makoto Samukawa, Hidekazu Suzuki, Motoi Kuwahara, Makito Hirano, Noriko Noguchi, Susumu Kusunoki

Neuroscience research　128　58-62　2018/03

DOI： 10.1016/j.neures.2017.06.008 　

ISSN： 0168-0102
Pleckstrin homology domain of p210 BCR-ABL interacts with cardiolipin to regulate its mitochondrial translocation and subsequent mitophagy Peer-reviewed

Shimasaki, K., Watanabe-Takahashi, M., Umeda, M., Funamoto, S., Saito, Y., Noguchi, N., Kumagai, K., Hanada, K., Tsukahara, F., Maru, Y., Shibata, N., Naito, M., Nishikawa, K.

Genes to Cells　23　(1)　22-34　2018
Publisher: Wiley
DOI： 10.1111/gtc.12544 　

ISSN： 1356-9597
PARK7 modulates autophagic proteolysis through binding to the N-terminally arginylated form of the molecular chaperone HSPA5 Peer-reviewed

Lee, D.-H., Kim, D., Kim, S.T., Jeong, S., Kim, J.L., Shim, S.M., Heo, A.J., Song, X., Guo, Z.S., Bartlett, D.L., Oh, S.C., Lee, J., Saito, Y., Kim, B.Y., Kwon, Y.T., Lee, Y.J.

Autophagy　14　(11)　1870-1885　2018

DOI： 10.1080/15548627.2018.1491212 　

ISSN： 1554-8627
Hydrogen peroxide-reducing factor released by PC12D cells increases cell tolerance against oxidative stress Peer-reviewed

Muraishi, A., Haneta, E., Saito, Y., Hitomi, Y., Sano, M., Noguchi, N.

Biological and Pharmaceutical Bulletin　41　(5)　777-785　2018

DOI： 10.1248/bpb.b18-00016 　

ISSN： 0918-6158

eISSN： 1347-5215
Comparison of human selenoprotein P determinants in serum between our original methods and commercially available kits Peer-reviewed

Saito, Y., Misu, H., Takayama, H., Takashima, S.-I., Usui, S., Takamura, M., Kaneko, S., Takamura, T., Noguchi, N.

Biological and Pharmaceutical Bulletin　41　(5)　828-832　2018
Publisher: Pharmaceutical Society of Japan
DOI： 10.1248/bpb.b18-00046 　

ISSN： 0918-6158

eISSN： 1347-5215
6-Hydroxydopamine induces secretion of PARK7/DJ-1 via autophagy-based unconventional secretory pathway Peer-reviewed

Urano, Y., Mori, C., Fuji, A., Konno, K., Yamamoto, T., Yashirogi, S., Ando, M., Saito, Y., Noguchi, N.

Autophagy　14　(11)　1943-1958　2018

DOI： 10.1080/15548627.2018.1493043 　

ISSN： 1554-8627
Tocopherol suppresses 24(S)-hydroxycholesterol-induced cell death via inhibition of CaMKII phosphorylation International-journal Peer-reviewed

Kimura, Y., Asa, M., Urano, Y., Saito, Y., Nishikawa, K., Noguchi, N.

Biochimie　153　203-209　2018
Publisher: Elsevier {BV}
DOI： 10.1016/j.biochi.2018.07.004 　

ISSN： 0300-9084
Selenoprotein P-neutralizing antibodies improve insulin secretion and glucose sensitivity in type 2 diabetes mouse models Peer-reviewed

Yuichiro Mita, Kaho Nakayama, Shogo Inari, Yukina Nishito, Yuya Yoshioka, Naoko Sakai, Kanade Sotani, Takahiro Nagamura, Yuki Kuzuhara, Kumi Inagaki, Miki Iwasaki, Hirofumi Misu, Masaya Ikegawa, Toshinari Takamura, Noriko Noguchi, Yoshiro Saito

NATURE COMMUNICATIONS　8　(1)　2017/11

DOI： 10.1038/s41467-017-01863-z 　

ISSN： 2041-1723
Eicosapentaenoic acid down-regulates expression of the selenoprotein P gene by inhibiting SREBP-1c protein independently of the AMP-activated protein kinase pathway in H4IIEC3 hepatocytes

Natsumi Tajima-Shirasaki, Kiyo-aki Ishil, Hiroaki Takayama, Takayoshi Shirasaki, Hisakazu Iwama, Keita Chikamoto, Yoshiro Saito, Yasumasa Iwasaki, Atsushi Teraguchi, Fei Lan, Akihiro Kikuchi, Yumie Takeshita, Koji Murao, Seiichi Matsugo, Shuichi Kaneko, Hirofumi Misu, Toshinari Takamura

JOURNAL OF BIOLOGICAL CHEMISTRY　292　(26)　10791-10800　2017/06

DOI： 10.1074/jbc.M116.747006 　

ISSN： 0021-9258

eISSN： 1083-351X
Effect of vitamin E on 24(S)-hydroxycholesterol-induced necroptosis-like cell death and apoptosis

Takaya Nakazawa, Yuta Miyanoki, Yasuomi Urano, Madoka Uehara, Yoshiro Saito, Noriko Noguchi

JOURNAL OF STEROID BIOCHEMISTRY AND MOLECULAR BIOLOGY　169　69-76　2017/05

DOI： 10.1016/j.jsbmb.2016.03.003 　

ISSN： 0960-0760
Deficiency of the hepatokine selenoprotein P increases responsiveness to exercise in mice through upregulation of reactive oxygen species and AMP-activated protein kinase in muscle Peer-reviewed

Hirofumi Misu, Hiroaki Takayama, Yoshiro Saito, Yuichiro Mita, Akihiro Kikuchi, Kiyo-aki Ishii, Keita Chikamoto, Takehiro Kanamori, Natsumi Tajima, Fei Lan, Yumie Takeshita, Masao Honda, Mutsumi Tanaka, Seiji Kato, Naoto Matsuyama, Yuya Yoshioka, Kaito Iwayama, Kumpei Tokuyama, Nobuhiko Akazawa, Seiji Maeda, Kazuhiro Takekoshi, Seiichi Matsugo, Noriko Noguchi, Shuichi Kaneko, Toshinari Takamura

NATURE MEDICINE　23　(4)　508-+　2017/04

DOI： 10.1038/nm.4295 　

ISSN： 1078-8956

eISSN： 1546-170X
Interleukin-27 Enhances the Potential of Reactive Oxygen Species Generation from Monocyte-derived Macrophages and Dendritic cells by Induction of p47(phox) Peer-reviewed

Bharatwaj Sowrirajan, Yoshiro Saito, Deepak Poudyal, Qian Chen, Hongyan Sui, Suk See DeRavin, Hiromi Imamichi, Toyotaka Sato, Douglas B. Kuhns, Noriko Noguchi, Harry L. Malech, H. Clifford Lane, Tomozumi Imamichi

SCIENTIFIC REPORTS　7　43441　2017/02

DOI： 10.1038/srep43441 　

ISSN： 2045-2322
DJ-1 as a biomarker of Parkinson’s disease Peer-reviewed

Yoshiro Saito

Advances in Experimental Medicine and Biology　1037　149-171　2017
Publisher: Springer New York LLC
DOI： 10.1007/978-981-10-6583-5_10 　

ISSN： 2214-8019 0065-2598
Oxidized Lipoprotein as a Major Vessel Cell Proliferator in Oxidized Human Serum

Yoshiro Saito, Noriko Noguchi

PLOS ONE　11　(8)　2016/08

DOI： 10.1371/journal.pone.0160530 　

ISSN： 1932-6203
Oxidation and interaction of DJ-1 with 20S proteasome in the erythrocytes of early stage Parkinson's disease patients

Yoshiro Saito, Yoko Akazawa-Ogawa, Akihiro Matsumura, Kazumasa Saigoh, Sayoko Itoh, Kenta Sutou, Mayuka Kobayashi, Yuichiro Mita, Mototada Shichiri, Shin Hisahara, Yasuo Hara, Harutoshi Fujimura, Hiroyuki Takamatsu, Yoshihisa Hagihara, Yasukazu Yoshida, Takao Hamakubo, Susumu Kusunoki, Shun Shimohama, Noriko Noguchi

SCIENTIFIC REPORTS　6　2016/07

DOI： 10.1038/srep30793 　

ISSN： 2045-2322
Development of a Sol Particle Homogeneous Immunoassay for Measuring Full-Length Selenoprotein P in Human Serum

Mutsumi Tanaka, Yoshiro Saito, Hirofumi Misu, Seiji Kato, Yuki Kita, Yumie Takeshita, Takehiro Kanamori, Toru Nagano, Masatoshi Nakagen, Takeshi Urabe, Toshinari Takamura, Shuichi Kaneko, Kazuhiko Takahashi, Naoto Matsuyama

JOURNAL OF CLINICAL LABORATORY ANALYSIS　30　(2)　114-122　2016/03

DOI： 10.1002/jcla.21824 　

ISSN： 0887-8013

eISSN： 1098-2825
The protective role of DJ-1 in ultraviolet-induced damage of human skin: DJ-1 levels in the stratum corneum as an indicator of antioxidative defense

Shioji Ishiwatari, Minako Takahashi, Chie Yasuda, Maho Nakagawa, Yoshiro Saito, Noriko Noguchi, Shoko Matsukuma

ARCHIVES OF DERMATOLOGICAL RESEARCH　307　(10)　925-935　2015/12

DOI： 10.1007/s00403-015-1605-8 　

ISSN： 0340-3696

eISSN： 1432-069X
Enhancement of lipid peroxidation and its amelioration by vitamin E in a subject with mutations in the SBP2 gene

Yoshiro Saito, Mototada Shichiri, Takashi Hamajima, Noriko Ishida, Yuichiro Mita, Shohei Nakao, Yoshihisa Hagihara, Yasukazu Yoshida, Kazuhiko Takahashi, Etsuo Niki, Noriko Noguchi

JOURNAL OF LIPID RESEARCH　56　(11)　2172-2182　2015/11

DOI： 10.1194/jlr.M059105 　

ISSN： 0022-2275

eISSN： 1539-7262
New aspects of 24(S)-hydroxycholesterol in modulating neuronal cell death

Noriko Noguchi, Yasuomi Urano, Wakako Takabe, Yoshiro Saito

FREE RADICAL BIOLOGY AND MEDICINE　87　366-372　2015/10

DOI： 10.1016/j.freeradbiomed.2015.06.036 　

ISSN： 0891-5849

eISSN： 1873-4596
24(S)-Hydroxycholesterol induces RIPK1-dependent but MLKL-independent cell death in the absence of caspase-8

Diep-Khanh Ho Vo, Yasuomi Urano, Wakako Takabe, Yoshiro Saito, Noriko Noguchi

STEROIDS　99　230-237　2015/07

DOI： 10.1016/j.steroids.2015.02.007 　

ISSN： 0039-128X

eISSN： 1878-5867
Selenoprotein P as a diabetes-associated hepatokine that impairs angiogenesis by inducing VEGF resistance in vascular endothelial cells

Kazuhide Ishikura, Hirofumi Misu, Masafumi Kumazaki, Hiroaki Takayama, Naoto Matsuzawa-Nagata, Natsumi Tajima, Keita Chikamoto, Fei Lan, Hitoshi Ando, Tsuguhito Ota, Masaru Sakurai, Yumie Takeshita, Kenichiro Kato, Akio Fujimura, Ken-ichi Miyamoto, Yoshiro Saito, Satomi Kameo, Yasuo Okamoto, Yoh Takuwa, Kazuhiko Takahashi, Hiroyasu Kidoya, Nobuyuki Takakura, Shuichi Kaneko, Toshinari Takamura

DIABETOLOGIA　57　(9)　1968-1976　2014/09

DOI： 10.1007/s00125-014-3306-9 　

ISSN： 0012-186X

eISSN： 1432-0428
LECT2 Functions as a Hepatokine That Links Obesity to Skeletal Muscle Insulin Resistance

Fei Lan, Hirofumi Misu, Keita Chikamoto, Hiroaki Takayama, Akihiro Kikuchi, Kensuke Mohri, Noboru Takata, Hiroto Hayashi, Naoto Matsuzawa-Nagata, Yumie Takeshita, Hiroyo Noda, Yukako Matsumoto, Tsuguhito Ota, Toru Nagano, Masatoshi Nakagen, Ken-ichi Miyamoto, Kanako Takatsuki, Toru Seo, Kaito Iwayama, Kunpei Tokuyama, Seiichi Matsugo, Hong Tang, Yoshiro Saito, Satoshi Yamagoe, Shuichi Kaneko, Toshinari Takamura

DIABETES　63　(5)　1649-1664　2014/05

DOI： 10.2337/db13-0728 　

ISSN： 0012-1797

eISSN： 1939-327X
Oxidized DJ-1 as a possible biomarker of Parkinson's disease

Yoshiro Saito

JOURNAL OF CLINICAL BIOCHEMISTRY AND NUTRITION　54　(3)　138-144　2014/05

DOI： 10.3164/jcbn.13-108 　

ISSN： 0912-0009

eISSN： 1880-5086
LECT2 functions as a hepatokine that links obesity to skeletal muscle insulin resistance. International-journal

Fei Lan, Hirofumi Misu, Keita Chikamoto, Hiroaki Takayama, Akihiro Kikuchi, Kensuke Mohri, Noboru Takata, Hiroto Hayashi, Naoto Matsuzawa-Nagata, Yumie Takeshita, Hiroyo Noda, Yukako Matsumoto, Tsuguhito Ota, Toru Nagano, Masatoshi Nakagen, Ken-ichi Miyamoto, Kanako Takatsuki, Toru Seo, Kaito Iwayama, Kunpei Tokuyama, Seiichi Matsugo, Hong Tang, Yoshiro Saito, Satoshi Yamagoe, Shuichi Kaneko, Toshinari Takamura

Diabetes　63　(5)　1649-64　2014/05
Publisher: American Diabetes Association
DOI： 10.2337/db13-0728 　

ISSN： 1939-327x

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Recent articles have reported an association between fatty liver disease and systemic insulin resistance in humans, but the causal relationship remains unclear. The liver may contribute to muscle insulin resistance by releasing secretory proteins called hepatokines. Here we demonstrate that leukocyte cell-derived chemotaxin 2 (LECT2), an energy-sensing hepatokine, is a link between obesity and skeletal muscle insulin resistance. Circulating LECT2 positively correlated with the severity of both obesity and insulin resistance in humans. LECT2 expression was negatively regulated by starvation-sensing kinase adenosine monophosphate-activated protein kinase in H4IIEC hepatocytes. Genetic deletion of LECT2 in mice increased insulin sensitivity in the skeletal muscle. Treatment with recombinant LECT2 protein impaired insulin signaling via phosphorylation of Jun NH2-terminal kinase in C2C12 myocytes. These results demonstrate the involvement of LECT2 in glucose metabolism and suggest that LECT2 may be a therapeutic target for obesity-associated insulin resistance.
Diverse functions of 24(S)-hydroxycholesterol in the brain

Noriko Noguchi, Yoshiro Saito, Yasuomi Urano

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS　446　(3)　692-696　2014/04

DOI： 10.1016/j.bbrc.2014.02.010 　

ISSN： 0006-291X

eISSN： 1090-2104
7-Hydroxycholestrol as a possible biomarker of cellular lipid peroxidation: Difference between cellular and plasma lipid peroxidation

Yoshiro Saito, Noriko Noguchi

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS　446　(3)　741-744　2014/04

DOI： 10.1016/j.bbrc.2013.12.083 　

ISSN： 0006-291X

eISSN： 1090-2104
パーキンソン病における酸化DJ-1測定のバイオマーカーとしての意義の検討 Peer-reviewed

小川郁子, 斎藤芳郎, 西郷和真, 細井幸恵, 三井良之, 野口範子, 楠進

Brain and Nerve　66　471-477　2014
The significance of oxidized DJ-1 protein (oxDJ-1) as a biomarker for parkinson's disease

Ikuko Ogawa, Yoshiro Saito, Kazumasa Saigoh, Yoshie Hosoi, Yoshiyuki Mitsui, Noriko Noguchi, Susumu Kusunoki

Brain and Nerve　66　(4)　471-477　2014
Publisher: Igaku-Shoin Ltd
ISSN： 1881-6096
Adaptive responses induced by 24S-hydroxycholesterol through liver X receptor pathway reduce 7-ketocholesterol-caused neuronal cell death

Akishi Okabe, Yasuomi Urano, Sayoko Itoh, Naoto Suda, Rina Kotani, Yuki Nishimura, Yoshiro Saito, Noriko Noguchi

REDOX BIOLOGY　2　28-35　2014

DOI： 10.1016/j.redox.2013.11.007 　

ISSN： 2213-2317
Induction of apoptosis and necroptosis by 24(S)-hydroxycholesterol is dependent on activity of acyl-CoA: cholesterol acyltransferase 1

K. Yamanaka, Y. Urano, W. Takabe, Y. Saito, N. Noguchi

CELL DEATH & DISEASE　5　2014/01

DOI： 10.1038/cddis.2013.524 　

ISSN： 2041-4889
Immunostaining of oxidized DJ-1 in human and mouse brains

Yoshiro Saito, Tomohiro Miyasaka, Hiroyuki Hatsuta, Kazuko Takahashi-Niki, Kojiro Hayashi, Yuichiro Mita, Osamu Kusano-Arai, Hiroko Iwanari, Hiroyoshi Ariga, Takao Hamakubo, Yasukazu Yoshida, Etsuo Niki, Shigeo Murayama, Yasuo Ihara, Noriko Noguchi

Journal of Neuropathology and Experimental Neurology　73　(7)　714-728　2014
Publisher: Lippincott Williams and Wilkins
DOI： 10.1097/NEN.0000000000000087 　

ISSN： 1554-6578 0022-3069
Metformin Suppresses Expression of the Selenoprotein P Gene via an AMP-activated Kinase (AMPK)/FoxO3a Pathway in H4IIEC3 Hepatocytes

Hiroaki Takayama, Hirofumi Misu, Hisakazu Iwama, Keita Chikamoto, Yoshiro Saito, Koji Murao, Atsushi Teraguchi, Fei Lan, Akihiro Kikuchi, Reina Saito, Natsumi Tajima, Takayoshi Shirasaki, Seiichi Matsugo, Ken-ichi Miyamoto, Shuichi Kaneko, Toshinari Takamura

JOURNAL OF BIOLOGICAL CHEMISTRY　289　(1)　335-345　2014/01

DOI： 10.1074/jbc.M113.479386 　

ISSN： 0021-9258

eISSN： 1083-351X
The significance of oxidized DJ-1 protein (oxDJ-1) as a biomarker for parkinson's disease Peer-reviewed

Ikuko Ogawa, Yoshiro Saito, Kazumasa Saigoh, Yoshie Hosoi, Yoshiyuki Mitsui, Noriko Noguchi, Susumu Kusunoki

Brain and Nerve　66　(4)　471-477　2014
Publisher: Igaku-Shoin Ltd
ISSN： 1881-6096
Oxidized DJ-1 Inhibits p53 by Sequestering p53 from Promoters in a DNA-Binding Affinity-Dependent Manner

Izumi Kato, Hiroshi Maita, Kazuko Takahashi-Niki, Yoshiro Saito, Noriko Noguchi, Sanae M. M. Iguchi-Ariga, Hiroyoshi Ariga

MOLECULAR AND CELLULAR BIOLOGY　33　(2)　340-359　2013/01

DOI： 10.1128/MCB.01350-12 　

ISSN： 0270-7306
Serum selenium and selenoprotein P in patients with silicosis

Basilua Andre Muzembo, Narongpon Dumavibhat, N'landu Roger Ngatu, Masamitsu Eitoku, Ryoji Hirota, Shinichi Kondo, Yoji Deguchi, Yoshiro Saito, Kazuhiko Takahashi, Narufumi Suganuma

JOURNAL OF TRACE ELEMENTS IN MEDICINE AND BIOLOGY　27　(1)　40-44　2013

DOI： 10.1016/j.jtemb.2012.05.003 　

ISSN： 0946-672X
Enhanced CD36 expression changes the role of Nrf2 activation from anti-atherogenic to pro-atherogenic in apoE-deficient mice

Hirotaka Sawada, Yoshiro Saito, Noriko Noguchi

ATHEROSCLEROSIS　225　(1)　83-90　2012/11

DOI： 10.1016/j.atherosclerosis.2012.08.023 　

ISSN： 0021-9150
Cytoprotective effects of geraniin against peroxynitrite- and peroxyl radical-induced cell death via free radical scavenging activity

Lai Teng Ling, Yoshiro Saito, Uma D. Palanisamy, Hwee Ming Cheng, Noriko Noguchi

FOOD CHEMISTRY　132　(4)　1899-1907　2012/06

DOI： 10.1016/j.foodchem.2011.12.024 　

ISSN： 0308-8146

eISSN： 1873-7072
Novel compound heterozygous mutations in the SBP2 gene: characteristic clinical manifestations and the implications of GH and triiodothyronine in longitudinal bone growth and maturation (vol 166, pg 757, 2012)

Takashi Hamajima, Yuichi Mushimoto, Hironori Kobayashi, Yoshiro Saito, Kaxumichi Onigata

EUROPEAN JOURNAL OF ENDOCRINOLOGY　166　(5)　957-957　2012/05

DOI： 10.1530/EJE-11-0812e 　

ISSN： 0804-4643
Inverse Correlation between Serum Levels of Selenoprotein P and Adiponectin in Patients with Type 2 Diabetes

Hirofumi Misu, Kazuhide Ishikura, Seiichiro Kurita, Yumie Takeshita, Tsuguhito Ota, Yoshiro Saito, Kazuhiko Takahashi, Shuichi Kaneko, Toshinari Takamura

PLOS ONE　7　(4)　e34952　2012/04

DOI： 10.1371/journal.pone.0034952 　

ISSN： 1932-6203
Novel compound heterozygous mutations in the SBP2 gene: characteristic clinical manifestations and the implications of GH and triiodothyronine in longitudinal bone growth and maturation

Takashi Hamajima, Yuichi Mushimoto, Hironori Kobayashi, Yoshiro Saito, Kazumichi Onigata

EUROPEAN JOURNAL OF ENDOCRINOLOGY　166　(4)　757-764　2012/04

DOI： 10.1530/EJE-11-0812 　

ISSN： 0804-4643
Selenoprotein P

Yoshiro Saito, Kazuhiko Takahashi

Advanced Topics in Science and Technology in China　77-88　2012
Publisher: Springer
DOI： 10.1007/978-3-642-22236-8_5 　

ISSN： 1995-6827 1995-6819
A novel fluorescent probe with high sensitivity and selective detection of lipid hydroperoxides in cells

Kazunori Yamanaka, Yoshiro Saito, Junji Sakiyama, Yuya Ohuchi, Fumio Oseto, Noriko Noguchi

RSC ADVANCES　2　(20)　7894-7900　2012

DOI： 10.1039/c2ra20816d 　

ISSN： 2046-2069
赤血球画分を用いた酸化DJ-1定量の検討

松村晃寛, 久原真, 齊藤正樹, 川又純, 今井富裕, 下濱俊, 斎藤芳郎, 野口範子, 二木鋭雄

臨床神経学　51　(12)　1266-1266　2011/12
Publisher: (一社)日本神経学会
ISSN： 0009-918X

eISSN： 1882-0654
Oxidation of DJ-1 Induced by 6-Hydroxydopamine Decreasing Intracellular Glutathione

Akiko Miyama, Yoshiro Saito, Kazunori Yamanaka, Kojiro Hayashi, Takao Hamakubo, Noriko Noguchi

PLOS ONE　6　(11)　e27883　2011/11

DOI： 10.1371/journal.pone.0027883 　

ISSN： 1932-6203
24(S)-Hydroxycholesterol Induces Neuronal Cell Death through Necroptosis, a Form of Programmed Necrosis

Kazunori Yamanaka, Yoshiro Saito, Tohru Yamamori, Yasuomi Urano, Noriko Noguchi

JOURNAL OF BIOLOGICAL CHEMISTRY　286　(28)　24666-24673　2011/07

DOI： 10.1074/jbc.M111.236273 　

ISSN： 0021-9258
Selenoprotein-P is Down-Regulated in Prostate Cancer, Which Results in Lack of Protection Against Oxidative Damage

Oscar Gonzalez-Moreno, Noemi Boque, Miriam Redrado, Fermin Milagro, Javier Campion, Tobias Endermann, Kazuhiko Takahashi, Yoshiro Saito, Raul Catena, Lutz Schomburg, Alfonso Calvo

PROSTATE　71　(8)　824-834　2011/06

DOI： 10.1002/pros.21298 　

ISSN： 0270-4137
Central nervous system-specific deletion of transcription factor Nrf1 causes progressive motor neuronal dysfunction

Akira Kobayashi, Takako Tsukide, Tomohiro Miyasaka, Tomoko Morita, Tatsuya Mizoroki, Yoshiro Saito, Yasuo Ihara, Akihiko Takashima, Noriko Noguchi, Akiyoshi Fukamizu, Yosuke Hirotsu, Makiko Ohtsuji, Fumiki Katsuoka, Masayuki Yamamoto

GENES TO CELLS　16　(6)　692-703　2011/06

DOI： 10.1111/j.1365-2443.2011.01522.x 　

ISSN： 1356-9597
Selenoprotein-P is Down-Regulated in Prostate Cancer, Which Results in Lack of Protection Against Oxidative Damage

Oscar Gonzalez-Moreno, Noemi Boque, Miriam Redrado, Fermin Milagro, Javier Campion, Tobias Endermann, Kazuhiko Takahashi, Yoshiro Saito, Raul Catena, Lutz Schomburg, Alfonso Calvo

PROSTATE　71　(8)　824-834　2011/06

DOI： 10.1002/pros.21298 　

ISSN： 0270-4137
alpha-Tocopheryl phosphate: Uptake, hydrolysis, and antioxidant action in cultured cells and mouse

Keiko Nishio, Noriko Ishida, Yoshiro Saito, Yoko Ogawa-Akazawa, Mototada Shichiri, Yasukazu Yoshida, Yoshihisa Hagihara, Noriko Noguchi, John Chirico, Jeffrey Atkinson, Etsuo Niki

FREE RADICAL BIOLOGY AND MEDICINE　50　(12)　1794-1800　2011/06

DOI： 10.1016/j.freeradbiomed.2011.03.021 　

ISSN： 0891-5849

eISSN： 1873-4596
Phosphorylation of p66shc mediates 6-hydroxydopamine cytotoxicity

Tohru Yamamori, Ayano Mizobata, Yoshiro Saito, Yasuomi Urano, Osamu Inanami, Kaikobad Irani, Noriko Noguchi

FREE RADICAL RESEARCH　45　(3)　342-350　2011/03

DOI： 10.3109/10715762.2010.532496 　

ISSN： 1071-5762
Phosphorylation of p66shc mediates 6-hydroxydopamine cytotoxicity

Tohru Yamamori, Ayano Mizobata, Yoshiro Saito, Yasuomi Urano, Osamu Inanami, Kaikobad Irani, Noriko Noguchi

FREE RADICAL RESEARCH　45　(3)　342-350　2011/03

DOI： 10.3109/10715762.2010.532496 　

ISSN： 1071-5762
Correlation between saliva cortisol concentration and sympathovagal balance before sleep in young male subjects

Yoshino Kohzoh, Saito Yoshiro, Jitousyo Mamiko, Yoshida Yasukazu

Stress Science Research　26　48-52　2011
Publisher: Public Health Research Foundation
DOI： 10.5058/stresskagakukenkyu.26.48 　

ISSN： 1341-9986

More details Close

The aim of this study is to investigate the correlation between saliva cortisol concentration and balance of autonomic nervous system (sympathovagal balance) before sleep in normal male subjects. The subjects (N=27) intermittently wore an ambulatory wearable device that records heart rate variability (RR-interval) for three days during daily life. Their saliva was sampled at each night before sleep. The cortisol concentration of each sample was quantified. The sympathovagal balance was evaluated by calculating the normalized high-frequency power (HFnu) of RR-interval variability that was measured from A+5 to A minutes (A=0, 5,..., 55) before the saliva sampling time. The correlation coefficients between high values of saliva cortisol concentration and the corresponding natural logarithm of HFnu were from -0.40 to -0.49 (p=0.006-0.034) when the values of A were 10, 15, 20, and 25. This result implies that hypothalamic-pituitary-adrenal (HPA) axis activity before sleep is significantly correlated with dominance of sympathetic nervous system activity with time lag of 10-30 minutes during relatively high stress condition.<br>
Cytoprotective effects of vitamin E homologues against glutamate-induced cell death in immature primary cortical neuron cultures: Tocopherols and tocotrienols exert similar effects by antioxidant function

Yoshiro Saito, Keiko Nishio, Yoko Ogawa Akazawa, Kazunori Yamanaka, Akiko Miyama, Yasukazu Yoshida, Noriko Noguchi, Etsuo Niki

FREE RADICAL BIOLOGY AND MEDICINE　49　(10)　1542-1549　2010/11

DOI： 10.1016/j.freeradbiomed.2010.08.016 　

ISSN： 0891-5849
A Liver-Derived Secretory Protein, Selenoprotein P, Causes Insulin Resistance

Hirofumi Misu, Toshinari Takamura, Hiroaki Takayama, Hiroto Hayashi, Naoto Matsuzawa-Nagata, Seiichiro Kurita, Kazuhide Ishikura, Hitoshi Ando, Yumie Takeshita, Tsuguhito Ota, Masaru Sakurai, Tatsuya Yamashita, Eishiro Mizukoshi, Taro Yamashita, Masao Honda, Ken-ichi Miyamoto, Tetsuya Kubota, Naoto Kubota, Takashi Kadowaki, Han-Jong Kim, In-Kyu Lee, Yasuhiko Minokoshi, Yoshiro Saito, Kazuhiko Takahashi, Yoshihiro Yamada, Nobuyuki Takakura, Shuichi Kaneko

CELL METABOLISM　12　(5)　483-495　2010/11

DOI： 10.1016/j.cmet.2010.09.015 　

ISSN： 1550-4131
Cytoprotective effects of vitamin E homologues against glutamate-induced cell death in immature primary cortical neuron cultures: Tocopherols and tocotrienols exert similar effects by antioxidant function

Yoshiro Saito, Keiko Nishio, Yoko Ogawa Akazawa, Kazunori Yamanaka, Akiko Miyama, Yasukazu Yoshida, Noriko Noguchi, Etsuo Niki

FREE RADICAL BIOLOGY AND MEDICINE　49　(10)　1542-1549　2010/11

DOI： 10.1016/j.freeradbiomed.2010.08.016 　

ISSN： 0891-5849
Elevation of oxidized DJ-1 in the brain and erythrocytes of Parkinson disease model animals

Yoko Ogawa Akazawa, Yoshiro Saito, Takao Hamakubo, Yoshinori Masuo, Yasukazu Yoshida, Keiko Nishio, Mototada Shichiri, Tomohiro Miyasaka, Hiroko Iwanari, Yasuhiro Mochizuki, Tatsuhiko Kodama, Noriko Noguchi, Etsuo Niki

NEUROSCIENCE LETTERS　483　(3)　201-205　2010/10

DOI： 10.1016/j.neulet.2010.08.007 　

ISSN： 0304-3940
Action of 6-amino-3-pyridinols as novel antioxidants against free radicals and oxidative stress in solution, plasma, and cultured cells

Yo Omata, Yoshiro Saito, Yasukazu Yoshida, Byeong-Seon Jeong, Remigiusz Serwa, Tae-gyu Nam, Ned A. Porter, Etsuo Niki

FREE RADICAL BIOLOGY AND MEDICINE　48　(10)　1358-1365　2010/05

DOI： 10.1016/j.freeradbiomed.2010.02.018 　

ISSN： 0891-5849
Proteomic characterization of the striatum and midbrain treated with 6-hydroxydopamine: Alteration of 58-kDa glucose-regulated protein and C/EBP homologous protein

Yoko Ogawa Akazawa, Yoshiro Saito, Keiko Nishio, Masanori Horie, Tomoya Kinumi, Yoshinori Masuo, Yasukazu Yoshida, Hitoshi Ashida, Etsuo Niki

FREE RADICAL RESEARCH　44　(4)　410-421　2010/04

DOI： 10.3109/10715760903536349 　

ISSN： 1071-5762

eISSN： 1029-2470
Hydroxyoctadecadienoic acid as a potential biomarker for oxidative stress in patients with chronic hepatitis C

Yasukazu Yoshida, Yasuharu Imai, Yoshiyuki Sawai, Yoshiro Saito, Jiaofei Cao, Kazuto Fukuda, Etsuo Niki

JOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY　25　(1)　107-115　2010/01

DOI： 10.1111/j.1440-1746.2009.05928.x 　

ISSN： 0815-9319
The role of alpha-tocopherol in motor hypofunction with aging in alpha-tocopherol transfer protein knockout mice as assessed by oxidative stress biomarkers

Yasukazu Yoshida, Nanako Itoh, Mieko Hayakawa, Yoko Habuchi, Yoshiro Saito, Yoshitane Tsukamoto, Osamu Cynshi, Kou-ichi Jishage, Hiroyuki Arai, Etsuo Niki

JOURNAL OF NUTRITIONAL BIOCHEMISTRY　21　(1)　66-76　2010/01

DOI： 10.1016/j.jnutbio.2008.10.006 　

ISSN： 0955-2863
The role of alpha-tocopherol in motor hypofunction with aging in alpha-tocopherol transfer protein knockout mice as assessed by oxidative stress biomarkers

Yasukazu Yoshida, Nanako Itoh, Mieko Hayakawa, Yoko Habuchi, Yoshiro Saito, Yoshitane Tsukamoto, Osamu Cynshi, Kou-ichi Jishage, Hiroyuki Arai, Etsuo Niki

JOURNAL OF NUTRITIONAL BIOCHEMISTRY　21　(1)　66-76　2010/01

DOI： 10.1016/j.jnutbio.2008.10.006 　

ISSN： 0955-2863
Hydroxyoctadecadienoic acid as a potential biomarker for oxidative stress in patients with chronic hepatitis C

Yasukazu Yoshida, Yasuharu Imai, Yoshiyuki Sawai, Yoshiro Saito, Jiaofei Cao, Kazuto Fukuda, Etsuo Niki

JOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY　25　(1)　107-115　2010/01

DOI： 10.1111/j.1440-1746.2009.05928.x 　

ISSN： 0815-9319
Preparation and application of monoclonal antibodies against oxidized DJ-1. Significant elevation of oxidized DJ-1 in erythrocytes of early-stage Parkinson disease patients

Yoshiro Saito, Takao Hamakubo, Yasukazu Yoshida, Yoko Ogawa, Yasuo Hara, Harutoshi Fujimura, Yasuharu Imai, Hiroko Iwanari, Yasuhiro Mochizuki, Mototada Shichiri, Keiko Nishio, Tomoya Kinumi, Noriko Noguchi, Tatsuhiko Kodama, Etsuo Niki

NEUROSCIENCE LETTERS　465　(1)　1-5　2009/11

DOI： 10.1016/j.neulet.2009.08.074 　

ISSN： 0304-3940
Antioxidant action of sugar-pendant C-60 fullerenes

Masanori Horie, Akiko Fukuhara, Yoshiro Saito, Yasukazu Yoshida, Hiroe Sato, Hiromi Ohi, Makoto Obata, Yuji Mikata, Shigenobu Yano, Etsuo Niki

BIOORGANIC & MEDICINAL CHEMISTRY LETTERS　19　(20)　5902-5904　2009/10

DOI： 10.1016/j.bmcl.2009.08.067 　

ISSN： 0960-894X
Antioxidant action of sugar-pendant C-60 fullerenes

Masanori Horie, Akiko Fukuhara, Yoshiro Saito, Yasukazu Yoshida, Hiroe Sato, Hiromi Ohi, Makoto Obata, Yuji Mikata, Shigenobu Yano, Etsuo Niki

BIOORGANIC & MEDICINAL CHEMISTRY LETTERS　19　(20)　5902-5904　2009/10

DOI： 10.1016/j.bmcl.2009.08.067 　

ISSN： 0960-894X
Assessment of the antioxidant capacity of a fermented grain food product, Antioxidant Biofactor (AOB), by using pyranine and pyrogallol red as a combined probe

Yo Omata, Yoko Ogawa, Yoshiro Saito, Yasukazu Yoshida, Etsuo Niki

FOOD CHEMISTRY　114　(2)　429-433　2009/05

DOI： 10.1016/j.foodchem.2008.09.066 　

ISSN： 0308-8146
Characterization of cellular uptake and distribution of coenzyme Q(10) and vitamin E in PC12 cells

Yoshiro Saito, Akiko Fukuhara, Keiko Nishio, Mieko Hayakawa, Yoko Ogawa, Hirokazu Sakamoto, Kenji Fujii, Yasukazu Yoshida, Etsuo Niki

JOURNAL OF NUTRITIONAL BIOCHEMISTRY　20　(5)　350-357　2009/05

DOI： 10.1016/j.jnutbio.2008.04.005 　

ISSN： 0955-2863
Characterization of cellular uptake and distribution of coenzyme Q(10) and vitamin E in PC12 cells

Yoshiro Saito, Akiko Fukuhara, Keiko Nishio, Mieko Hayakawa, Yoko Ogawa, Hirokazu Sakamoto, Kenji Fujii, Yasukazu Yoshida, Etsuo Niki

JOURNAL OF NUTRITIONAL BIOCHEMISTRY　20　(5)　350-357　2009/05

DOI： 10.1016/j.jnutbio.2008.04.005 　

ISSN： 0955-2863
Assessment of the antioxidant capacity of a fermented grain food product, Antioxidant Biofactor (AOB), by using pyranine and pyrogallol red as a combined probe

Yo Omata, Yoko Ogawa, Yoshiro Saito, Yasukazu Yoshida, Etsuo Niki

FOOD CHEMISTRY　114　(2)　429-433　2009/05

DOI： 10.1016/j.foodchem.2008.09.066 　

ISSN： 0308-8146
Sustainable and practical degradation of intact chicken feathers by cultivating a newly isolated thermophilic Meiothermus ruber H328

Tatsunobu Matsui, Yukie Yamada, Hideki Mitsuya, Yasushi Shigeri, Yasukazu Yoshida, Yoshiro Saito, Hiroshi Matsui, Kunihiko Watanabe

APPLIED MICROBIOLOGY AND BIOTECHNOLOGY　82　(5)　941-950　2009/04

DOI： 10.1007/s00253-009-1880-4 　

ISSN： 0175-7598

eISSN： 1432-0614
Protein Adsorption of Ultrafine Metal Oxide and Its Influence on Cytotoxicity toward Cultured Cells

Masanori Horie, Keiko Nishio, Katsuhide Fujita, Shigehisa Endoh, Arisa Miyauchi, Yoshiro Saito, Hitoshi Iwahashi, Kazuhiro Yamamoto, Hideki Murayama, Haiime Nakano, Naoki Nanashima, Etsuo Niki, Yasukazu Yoshida

CHEMICAL RESEARCH IN TOXICOLOGY　22　(3)　543-553　2009/03

DOI： 10.1021/tx800289z 　

ISSN： 0893-228X
Hydroxyoctadecadienoic acid and oxidatively modified peroxiredoxins in the blood of Alzheimer's disease patients and their potential as biomarkers

Yasukazu Yoshida, Atsushi Yoshikawa, Tomoya Kinumi, Yoko Ogawa, Yoshiro Saito, Kazuyuki Ohara, Hirokazu Yamamoto, Yasuharu Imai, Etsuo Niki

NEUROBIOLOGY OF AGING　30　(2)　174-185　2009/02

DOI： 10.1016/j.neurobiolaging.2007.06.012 　

ISSN： 0197-4580

eISSN： 1558-1497
A gene expression profiling approach to study the influence of ultrafine particles on rat lungs

Katsuhide Fujita, Yasuo Morimoto, Akira Ogami, Isamu Tanaka, Shigehisa Endoh, Kunio Uchida, Hiroaki Tao, Mikio Akasaka, Masaharu Inada, Kazuhiro Yamamoto, Hiroko Fukui, Mieko Hayakawa, Masanori Horie, Yoshiro Saito, Yasukazu Yoshida, Hitoshi Iwahashi, Etsuo Niki, Junko Nakanishi

Atmospheric and Biological Environmental Monitoring　219-227　2009
Publisher: Springer Netherlands
DOI： 10.1007/978-1-4020-9674-7_14 　
Assessment of antioxidant capacity of fermented grain food product, Antioxidant Biofactor (AOB), by ORAC method and inhibition of lipid peroxidation

斎藤芳郎

Food Chemistry　(114)　429-433　2009

DOI： 10.1016/j.foodchem.2008.09.066 　
Characterization of novel furan compounds on the basis of their radical scavenging activity and cytoprotective effects against glutamate- and lipopolysaccharide-induced insults

Keiko Nishio, Akiko Fukuhara, Yo Omata, Yoshiro Saito, Shuuhei Yamaguchi, Hisatoyo Kato, Yasukazu Yoshida, Etsuo Niki

BIOORGANIC & MEDICINAL CHEMISTRY　16　(24)　10332-10337　2008/12

DOI： 10.1016/j.bmc.2008.10.038 　

ISSN： 0968-0896
Induction of adaptive response and enhancement of PC12 cell tolerance by lipopolysaccharide primarily through the upregulation of glutathione S-transferase A3 via Nrf2 activation Peer-reviewed

Yo Omata, Yoshiro Saito, Katsuhide Fujita, Yoko Ogawa, Keiko Nishio, Yasukazu Yoshida, Etsuo Niki

FREE RADICAL BIOLOGY AND MEDICINE　45　(10)　1437-1445　2008/11

DOI： 10.1016/j.freeradbiomed.2008.08.018 　

ISSN： 0891-5849
Assessment of radical scavenging capacity and lipid peroxidation inhibiting capacity of antioxidant

Etsuo Niki, Yo Omata, Akiko Fukuhara, Yoshiro Saito, Yasukazu Yoshida

JOURNAL OF AGRICULTURAL AND FOOD CHEMISTRY　56　(18)　8255-8260　2008/09

DOI： 10.1021/jf800605x 　

ISSN： 0021-8561
Effect of oxygen concentration on free radical-induced cytotoxicity

Zhi-Hua Chen, Yoshiro Saito, Yasukazu Yoshida, Etsuo Niki

BIOSCIENCE BIOTECHNOLOGY AND BIOCHEMISTRY　72　(6)　1491-1497　2008/06

DOI： 10.1271/bbb.80002 　

ISSN： 0916-8451

eISSN： 1347-6947
Simple assessment of radical scavenging capacity of beverages

Yo Omata, Yoshiro Saito, Yasukazu Yoshida, Etsuo Niki

JOURNAL OF AGRICULTURAL AND FOOD CHEMISTRY　56　(9)　3386-3390　2008/05

DOI： 10.1021/jf703771v 　

ISSN： 0021-8561
Antioxidant capacity of BO-653, 2,3-dihydro-5-hydroxy-4, 6-di-tert-butyl-2,2-dipentylbenzofuran, and uric acid as evaluated by ORAC method and inhibition of lipid peroxidation

Etsuo Niki, Akiko Fukuhara, Yo Omata, Yoshiro Saito, Yasukazu Yoshida

BIOORGANIC & MEDICINAL CHEMISTRY LETTERS　18　(7)　2464-2466　2008/04

DOI： 10.1016/j.bmcl.2008.02.038 　

ISSN： 0960-894X
Novel finding regarding cholesterol oxidation: Cholesterol is more susceptible to oxidation than linoleates in cultured cells under oxidative stress.

斎藤芳郎

International Arteriosclerosis Society (IAS) commentaries　2008
Induction of Adaptive Response and Enhancement of PC12 Cell Tolerance by Lipopolysaccharide Primarily Through the Upregulation of Glutathione S-Transferase A3 Via Nrf2 Activation

Yoshiro Saito, Yo Omata, Yasukazu Yoshida, Noriko Noguchi, Etsuo Niki

FREE RADICAL BIOLOGY AND MEDICINE　45　(45)　S37-S37　2008

DOI： 10.1016/j.freeradbiomed.2008.08.018 　

ISSN： 0891-5849
gamma-tocopheryl quinone, not alpha-tocopheryl quinone, induces adaptive response through up-regulation of cellular glutathione and cysteine availability via activation of ATF4

Yoko Ogawa, Yoshiro Saito, Keiko Nishio, Yasukazu Yoshida, Hitoshi Ashida, Etsuo Niki

FREE RADICAL RESEARCH　42　(7)　674-U17　2008

DOI： 10.1080/10715760802277396 　

ISSN： 1071-5762
Regulation of GCL activity and cellular glutathione through inhibition of ERK phosphorylation

Zhi-Hua Chen, Yoshiro Saito, Yasukazu Yoshida, Noriko Noguchi, Etsuo Niki

BIOFACTORS　33　(1)　1-11　2008

DOI： 10.1002/biof.5520330101 　

ISSN： 0951-6433
Chemical reactivities and physical effects in comparison between tocopherols and tocotrienols: Physiological significance and prospects as antioxidants

Yasukazu Yoshida, Yoshiro Saito, Leslie Sargent Jones, Yasushi Shigeri

JOURNAL OF BIOSCIENCE AND BIOENGINEERING　104　(6)　439-445　2007/12

DOI： 10.1263/jbb.104.439 　

ISSN： 1389-1723

eISSN： 1347-4421
Cholesterol is more susceptible to oxidation than linoleates in cultured cells under oxidative stress induced by selenium deficiency and free radicals

Yoshiro Saito, Yasukazu Yoshida, Etsuo Niki

FEBS LETTERS　581　(22)　4349-4354　2007/09

DOI： 10.1016/j.febslet.2007.08.010 　

ISSN： 0014-5793
Protective effects of 15-deoxy-Delta(12,14)-prostaglandin J(2) against glutamate-induced cell death in primary cortical neuron cultures: induction of adaptive response and enhancement of cell tolerance primarily through up-regulation of cellular glutathione

Yoshiro Saito, Keiko Nishio, Yumiko Numakawa, Yoko Ogawa, Yasukazu Yoshida, Noriko Noguchi, Etsuo Niki

JOURNAL OF NEUROCHEMISTRY　102　(5)　1625-1634　2007/09

DOI： 10.1111/j.1471-4159.2007.04701.x 　

ISSN： 0022-3042
Levels of lipid peroxidation in human plasma and erythrocytes: Comparison between fatty acids and cholesterol

Yasukazu Yoshida, Yoshiro Saito, Mieko Hayakawa, Yoko Habuchi, Yasuharu Imai, Yoshiyuki Sawai, Etsuo Niki

LIPIDS　42　(5)　439-449　2007/05

DOI： 10.1007/s11745-007-3037-5 　

ISSN： 0024-4201
Molecular mechanisms of 6-hydroxydopamine-induced cytotoxicity in PC12 cells: Involvement of hydrogen peroxide-dependent and -independent action

Yoshiro Saito, Keiko Nishio, Yoko Ogawa, Tomoya Kinumi, Yasukazu Yoshida, Yoshinori Masuo, Etsuo Niki

FREE RADICAL BIOLOGY AND MEDICINE　42　(5)　675-685　2007/03

DOI： 10.1016/j.freeradbiomed.2006.12.004 　

ISSN： 0891-5849
Assessment of antioxidative activity of extract from fermented grain food mixture using chemical and cellular systems

Yoko Ogawa, Yo Omata, Keiko Nishio, Yoshiro Saito, Yasukazu Yoshida, Etsuo Niki

BIOFACTORS　31　(3-4)　237-248　2007

ISSN： 0951-6433
Cytotoxic effects of various stressors on PC12 cells: Involvement of oxidative stress and effect of antioxidants

Rosaria Piga, Yoshiro Saito, Yasukazu Yoshida, Etsuo Niki

NEUROTOXICOLOGY　28　(1)　67-75　2007/01

DOI： 10.1016/j.neuro.2006.07.006 　

ISSN： 0161-813X
Assessment of antioxidative activity of extract from fermented grain food mixture using chemical and cellular systems Peer-reviewed

Yoko Ogawa, Yo Omata, Keiko Nishio, Yoshiro Saito, Yasukazu Yoshida, Etsuo Niki

BIOFACTORS　31　(3-4)　237-248　2007

DOI： 10.1002/biof.5520310311 　

ISSN： 0951-6433
Turning point in apoptosis/necrosis induced by hydrogen peroxide

Yoshiro Saito, Keiko Nishio, Yoko Ogawa, Junko Kimata, Tomoya Kinumi, Yasukazu Yoshida, Noriko Noguchi, Etsuo Niki

FREE RADICAL RESEARCH　40　(6)　619-630　2006/06

DOI： 10.1080/10715760600632552 　

ISSN： 1071-5762

eISSN： 1029-2470
Induction of Adaptive Response and Enhancement of PC12 Cell Tolerance by 7-Hydroxycholesterol and 15-Deoxy-Delta(12,14)-Prostaglandin J(2) through Up-regulation of Cellular Glutathione via Different Mechanisms

Zhi-Hua Chen, Yasukazu Yoshida, Yoshiro Saito, Azusa Sekine, Noriko Noguchi, Etsuo Niki

JOURNAL OF BIOLOGICAL CHEMISTRY　281　(20)　14440-14445　2006/05

DOI： 10.1074/jbc.M600260200 　

ISSN： 0021-9258
Adaptive response induced by lipid peroxidation products in cell cultures

ZH Chen, Y Yoshida, Y Saito, N Noguchi, E Niki

FEBS LETTERS　580　(2)　479-483　2006/01

DOI： 10.1016/j.febslet.2005.12.045 　

ISSN： 0014-5793
Lipid peroxidation: Mechanisms, inhibition, and biological effects

E Niki, Y Yoshida, Y Saito, N Noguchi

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS　338　(1)　668-676　2005/12

DOI： 10.1016/j.bbrc.2005.08.072 　

ISSN： 0006-291X
4-Hydroxynonenal induces adaptive response and enhances PC12 cell tolerance primarily through induction of thioredoxin reductase 1 via activation of Nrf2

ZH Chen, Y Saito, Y Yoshida, A Sekine, N Noguchi, E Niki

JOURNAL OF BIOLOGICAL CHEMISTRY　280　(51)　41921-41927　2005/12

DOI： 10.1074/jbc.M508556200 　

ISSN： 0021-9258
Proteomic characterization of oxidative dysfunction in human umbilical vein endothelial cells (HUVEC) induced by exposure to oxidized LDL

T Kinumi, Y Ogawa, J Kimata, Y Saito, Y Yoshida, E Niki

FREE RADICAL RESEARCH　39　(12)　1335-1344　2005/12

DOI： 10.1080/10715760500306695 　

ISSN： 1071-5762
Adaptation to hydrogen peroxide enhances PC12 cell tolerance against oxidative damage

ZH Chen, Y Yoshida, Y Saito, E Niki

NEUROSCIENCE LETTERS　383　(3)　256-259　2005/08

DOI： 10.1016/j.neulet.2005.04.022 　

ISSN： 0304-3940
Cytotoxic effect of formaldehyde with free radicals via increment of cellular reactive oxygen species

Y Saito, K Nishio, Y Yoshida, E Niki

TOXICOLOGY　210　(2-3)　235-245　2005/06

DOI： 10.1016/j.tox.2005.02.006 　

ISSN： 0300-483X
Characterization of monochloramine toxicity on PC12 cells and protective effect of tocopherol via antioxidative function

R Piga, Y Saito, ZH Chen, Y Yoshida, E Niki

ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS　436　(1)　101-109　2005/04

DOI： 10.1016/j.abb.2005.01.021 　

ISSN： 0003-9861
Domain structure of bi-functional selenoprotein P

Y Saito, N Sato, M Hirashima, G Takebe, S Nagasawa, E Niki, K Takahashi

Natural Antioxidants and Micronutrients　105-108　2005
Selenoprotein P, as a predictor for evaluating gemcitabine resistance in human pancreatic cancer cells

S Maehara, S Tanaka, M Shimada, K Shirabe, Y Saito, K Takahashi, Y Maehara

INTERNATIONAL JOURNAL OF CANCER　112　(2)　184-189　2004/11

DOI： 10.1002/ijc.20304 　

ISSN： 0020-7136
Domain structure of bi-functional selenoprotein P

Y Saito, N Sato, M Hirashima, G Takebe, S Nagasawa, K Takahashi

BIOCHEMICAL JOURNAL　381　(381)　841-846　2004/08

DOI： 10.1042/BJ20040328 　

ISSN： 0264-6021
Effects of a novel gaseous antioxidative system containing a rosemary extract on the oxidation induced by nitrogen dioxide and ultraviolet radiation

Y Saito, A Shiga, Y Yoshida, T Furuhashi, Y Fujita, E Niki

BIOSCIENCE BIOTECHNOLOGY AND BIOCHEMISTRY　68　(4)　781-786　2004/04

DOI： 10.1271/bbb.68.781 　

ISSN： 0916-8451

eISSN： 1347-6947
Application of water-soluble radical initiator, 2,2 '-azobis-[2-(2-imidazolin-2-yl)propane] dihydrochloride, to a study of oxidative stress

Y Yoshida, N Itoh, Y Saito, M Hayakawa, E Niki

FREE RADICAL RESEARCH　38　(4)　375-384　2004/04

DOI： 10.1080/1071576042000191763 　

ISSN： 1071-5762
DJ-1 has a role in antioxidative stress to prevent cell death (vol 5, pg 213, 2004)

T Taira, Y Saito, T Niki, SMM Iguchi-Ariga, K Takahashi, H Ariga

EMBO REPORTS　5　(4)　430-430　2004/04

DOI： 10.1038/sj.embor.7400143 　

ISSN： 1469-221X
DJ-1 has a role in antioxidative stress to prevent cell death

T Taira, Y Saito, T Niki, SMM Iguchi-Ariga, K Takahashi, H Ariga

EMBO REPORTS　5　(2)　213-218　2004/02

DOI： 10.1038/sj.embor.7400074 　

ISSN： 1469-221X
Effects of Volatile Constituents of the Rosemary Extract on the Oxidation Caused by Ultraviolet Radiation and Nitrogen Dioxide

斎藤芳郎

Aroma Research　(18)　118-122　2004
Characterization of cellular uptake and distribution of vitamin E

Y Saito, Y Yoshida, K Nishio, M Hayakawa, E Niki

VITAMIN E AND HEALTH　1031　(1031)　368-375　2004

DOI： 10.1196/annals.1331.047 　

ISSN： 0077-8923
Cell death caused by selenium deficiency and protective effect of antioxidants

Y Saito, Y Yoshida, T Akazawa, K Takahashi, E Niki

JOURNAL OF BIOLOGICAL CHEMISTRY　278　(41)　39428-39434　2003/10

DOI： 10.1074/jbc.M305542200 　

ISSN： 0021-9258
Identification of selenoprotein P fragments as a cell-death inhibitory factor

M Hirashima, T Naruse, H Maeda, C Nozaki, Y Saito, K Takahashi

BIOLOGICAL & PHARMACEUTICAL BULLETIN　26　(6)　794-798　2003/06

DOI： 10.1248/bpb.26.794 　

ISSN： 0918-6158
Identification of selenoprotein P fragments as a cell-death inhibitory factor Peer-reviewed

M Hirashima, T Naruse, H Maeda, C Nozaki, Y Saito, K Takahashi

BIOLOGICAL & PHARMACEUTICAL BULLETIN　26　(6)　794-798　2003/06

DOI： 10.1248/bpb.26.794 　

ISSN： 0918-6158
Identification of selenoprotein P fragments as a cell-death inhibitory factor

Masaki Hirashima, Takeshi Naruse, Hiroaki Maeda, Chikateru Nozaki, Yoshiro Saito, Kazuhiko Takahashi

Biological and Pharmaceutical Bulletin　26　(6)　794-798　2003
Publisher: Pharmaceutical Society of Japan
DOI： 10.1248/bpb.26.794 　

ISSN： 0918-6158
Characterization of selenoprotein P as a selenium supply protein

Y Saito, K Takahashi

EUROPEAN JOURNAL OF BIOCHEMISTRY　269　(22)　5746-5751　2002/11

DOI： 10.1046/j.1432-1033.2002.03298.x 　

ISSN： 0014-2956
A comparative study on the hydroperoxide and thiol specificity of the glutathione peroxidase family and selenoprotein P

G Takebe, J Yarimizu, Y Saito, T Hayashi, H Nakamura, J Yodoi, S Nagasawa, K Takahashi

JOURNAL OF BIOLOGICAL CHEMISTRY　277　(43)　41254-41258　2002/10

DOI： 10.1074/jbc.M202773200 　

ISSN： 0021-9258
Production and application of monoclonal antibodies to human selenoprotein P

Y Saito, Y Watanabe, E Saito, T Honjoh, K Takahashi

JOURNAL OF HEALTH SCIENCE　47　(4)　346-352　2001/08

DOI： 10.1248/jhs.47.346 　

ISSN： 1344-9702
Structure and function of human selenoprotein P Peer-reviewed

K Takahashi, Y Saito

SEIKAGAKU　73　(4)　261-264　2001/04

ISSN： 0037-1017
Selenoprotein P: Its structure and functions Peer-reviewed

Y. Saito, K. Takahashi

Journal of Health Science　46　(6)　409-413　2000
Publisher: Pharmaceutical Society of Japan
DOI： 10.1248/jhs.46.409 　

ISSN： 1344-9702
Selenoprotein P in human plasma as an extracellular phospholipid hydroperoxide glutathione peroxidase - Isolation and enzymatic characterization of human selenoprotein P

Y Saito, T Hayashi, A Tanaka, Y Watanabe, M Suzuki, E Saito, K Takahashi

JOURNAL OF BIOLOGICAL CHEMISTRY　274　(5)　2866-2871　1999/01

DOI： 10.1074/jbc.274.5.2866 　

ISSN： 0021-9258

Show all ︎Show first 5

Misc. 126

過酸化水素によるATPの減少はAMPKの活性化を介してSelenoprotein Pの発現を抑制する。

三田雄一郎, 細川萩月, 斎藤芳郎, 野口範子

日本酸化ストレス学会学術集会プログラム・抄録集　77th　2024
パーキンソン病で増加するDJ-1の翻訳後修飾に53番目のシステインが関与する

松田康平, 三田雄一郎, 浦野泰臣, 西郷和真, 斎藤芳郎, 野口範子

日本酸化ストレス学会学術集会プログラム・抄録集　77th　2024
肝蔵のフェロトーシス感受性におけるセレノプロテインP発現の意義

名取萌花, 有澤琴子, 斎藤芳郎

次世代を担う若手のためのファーマ・バイオフォーラム講演要旨集　21st　2022
グリオブラストーマ治療標的としてのSeP/ApoER2経路

杉浦ひかり, 清水未崎, 金子尚志, 外山喬士, 斎藤芳郎

次世代を担う若手のためのファーマ・バイオフォーラム講演要旨集　21st　2022
細胞外基質ネフロネクチンはCD4+T細胞内の活性酸素種(ROS)介したTh17/Tregバランス制御により自己免疫疾患増悪化に関与する

本田真知子, 斎藤芳郎, 今重之

日本薬学会年会要旨集　141年会　27P02-130　2021/03
Publisher: (公社)日本薬学会
ISSN： 0918-9823
【食と健康を結ぶメディカルサイエンス生体防御系を亢進し、健康の維持に働く分子機構】(第2章)食による生体防御系の活性化抗酸化セレノプロテインの機能と疾患食とセレンの代謝

斎藤芳郎

実験医学　38　(10)　1654-1662　2020/06
Publisher: (株)羊土社
ISSN： 0288-5514
硫黄代謝研究の最前線が切り拓く毒性学セレン-硫黄代謝の接点およびクロストーク生体内における識別とその制御

斎藤芳郎

The Journal of Toxicological Sciences　45　(Suppl.)　S15-S15　2020/06
Publisher: (一社)日本毒性学会
ISSN： 0388-1350

eISSN： 1880-3989
ミクログリアにおけるメチル水銀によるMAPキナーゼを介したTNF-α発現誘導機構

外山喬士, 星尚志, 斎藤芳郎, 永沼章, 黄基旭

The Journal of Toxicological Sciences　45　(Suppl.)　S129-S129　2020/06
Publisher: (一社)日本毒性学会
ISSN： 0388-1350

eISSN： 1880-3989
マウス脳内におけるTNF受容体3の発現細胞特定およびメチル水銀による中枢神経障害における役割の解明

角田洋平, 外山喬士, 永沼章, 斎藤芳郎, 黄基旭

The Journal of Toxicological Sciences　45　(Suppl.)　S134-S134　2020/06
Publisher: (一社)日本毒性学会
ISSN： 0388-1350

eISSN： 1880-3989
セレン含有タンパク質セレノプロテインPのセレン運搬活性における受容体ApoER2バリアントの関与

水野彩子, 堤良平, 斎藤芳郎

日本薬学会年会要旨集　140年会　26P-am155S　2020/03
Publisher: (公社)日本薬学会
ISSN： 0918-9823
ビタミンE類の多様な抗酸化作用アイソフォームによる細胞保護メカニズムの違い

斎藤芳郎

ビタミン　94　(2)　59-70　2020/02
Publisher: (公社)日本ビタミン学会
ISSN： 0006-386X
ホメオスタシスにおける活性酸素の功罪生活習慣病と抗酸化タンパク質セレノプロテインP

斎藤芳郎

日本運動生理学雑誌　26　(2)　45-49　2019/12
Publisher: 日本運動生理学会
ISSN： 1340-3036
角層DJ-1を用いた体内の酸化ストレス評価

高橋理子, 鈴木民恵, 石渡潮路, 村上礼一, 秋田美季, 宮川泰子, 三上正治, 八代壇, 斎藤芳郎, 野口範子, 松熊祥子

加齢皮膚医学セミナー　14　(2)　70-70　2019/12
Publisher: 加齢皮膚医学研究会
セレノプロテインPの機能と疾患疾患バイオマーカーとしての可能性

斎藤芳郎

生化学　91　(5)　686-690　2019/10
Publisher: (公社)日本生化学会
ISSN： 0037-1017
ビタミンE類の多様な抗酸化作用必須微量元素セレンとの関わり

斎藤芳郎

ビタミン　93　(9)　424-424　2019/09
Publisher: (公社)日本ビタミン学会
ISSN： 0006-386X
生体エネルギーと電子共役の複雑性制御生体内におけるセレン代謝とエネルギー産生

斎藤芳郎

日本生化学会大会プログラム・講演要旨集　92回　[2S18m-02]　2019/09
Publisher: (公社)日本生化学会
革新的治療法を生み出すセレノプロテイン研究抗酸化ヘパトカイン"セレノプロテインP"が惹起する全身の糖尿病関連病態

高山浩昭, 御簾博文, 斎藤芳郎, 篁俊成

日本生化学会大会プログラム・講演要旨集　92回　[3S15m-01]　2019/09
Publisher: (公社)日本生化学会
革新的治療法を生み出すセレノプロテイン研究肺動脈性肺高血圧症の新しい治療標的セレノプロテインP

佐藤公雄, 菊地順裕, 斎藤芳郎, 下川宏明

日本生化学会大会プログラム・講演要旨集　92回　[3S15m-02]　2019/09
Publisher: (公社)日本生化学会
角層DJ-1を用いた体内の酸化ストレス評価

高橋理子, 鈴木民恵, 石渡潮路, 村上礼一, 秋田美季, 宮川泰子, 三上正治, 八代壇, 斎藤芳郎, 野口範子, 松熊祥子

加齢皮膚医学セミナー　14　(1)　49-57　2019/06
Publisher: 加齢皮膚医学研究会
角層DJ-1を用いた体内の酸化ストレス評価

高橋理子, 鈴木民恵, 石渡潮路, 村上礼一, 秋田美季, 宮川泰子, 三上正治, 八代壇, 斎藤芳郎, 野口範子, 松熊祥子

加齢皮膚医学セミナー　14　(1)　68-68　2019/06
Publisher: 加齢皮膚医学研究会
革新的なレドックス研究から見えてきた生命科学の新世紀血漿セレン含有タンパク質セレノプロテインPによるレドックス制御メカニズムおよびその破綻と糖尿病

斎藤芳郎

日本生化学会大会プログラム・講演要旨集　91回　[2S08m-07]　2018/09
Publisher: (公社)日本生化学会
パーキンソン病のバイオマーカーへの期待

鈴木則宏, 斎藤芳郎, 関守信, 徳田隆彦

Frontiers in Parkinson Disease　11　(2)　63-75　2018/06
Publisher: (株)メディカルレビュー社
ISSN： 1883-0331
Serenoprotein P中和抗体を用いた糖尿病治療の開発

三田雄一郎, 中山華穂, 稲荷尚吾, 野口範子, 斎藤芳郎

日本内分泌学会雑誌　94　(1)　360-360　2018/04
Publisher: (一社)日本内分泌学会
ISSN： 0029-0661

eISSN： 2186-506X
インスリン抵抗性の病態から治療への展開ヘパトカインセレノプロテインPを標的とするインスリン抵抗性治療薬の開発を目指して

御簾博文, 三田雄一郎, 斎藤芳郎, 篁俊成

糖尿病　61　(Suppl.1)　S-29　2018/04
Publisher: (一社)日本糖尿病学会
ISSN： 0021-437X

eISSN： 1881-588X
インスリン抵抗性の病態から治療への展開ヘパトカインセレノプロテインPを標的とするインスリン抵抗性治療薬の開発を目指して

御簾博文, 三田雄一郎, 斎藤芳郎, 篁俊成

糖尿病　61　(Suppl.1)　S-29　2018/04
Publisher: (一社)日本糖尿病学会
ISSN： 0021-437X
発見から200年を迎えた必須微量元素セレン研究の最前線セレノプロテインPのセレン運搬作用と膵β細胞のレドックス制御

斎藤芳郎

日本薬学会年会要旨集　138年会　(1)　221-221　2018/03
Publisher: (公社)日本薬学会
ISSN： 0918-9823
【レドックス疾患学酸素・窒素・硫黄活性種はどう作用するのか、どこまで健康・疾患と関わるのか?】 (第2章)レドックスと疾患セレノプロテインPによるレドックス制御と2型糖尿病

斎藤芳郎, 野口範子, 御簾博文, 篁俊成

実験医学　36　(5)　753-759　2018/03
Publisher: (株)羊土社
ISSN： 0288-5514
膵β細胞モデルMIN6はセレノプロテインP発現を介して抗酸化システムを維持する

中尾昌平, 三田雄一郎, 斎藤芳郎, 野口範子

生命科学系学会合同年次大会　2017年度　[2P-0374]　2017/12
Publisher: 生命科学系学会合同年次大会運営事務局
膵β細胞モデルMIN6における過剰Selenoprotein Pによるセレン運搬作用を介したERストレス誘導メカニズムの解析

長村尭浩, 稲荷尚吾, 三田雄一郎, 野口範子, 斎藤芳郎

生命科学系学会合同年次大会　2017年度　[2P-1003]　2017/12
Publisher: 生命科学系学会合同年次大会運営事務局
non-coding RNAによるSelenoprotein P翻訳抑制メカニズムの解析

三田雄一郎, 斎藤芳郎, 内田理沙, 安原小百合, 横大路将, 野口範子

生命科学系学会合同年次大会　2017年度　[3P-0671]　2017/12
Publisher: 生命科学系学会合同年次大会運営事務局
糖尿病関連タンパク質Selenoprotein Pの翻訳を抑制する内在性long non-coding RNAの発現変化

内田理沙, 三田雄一郎, 横大路将, 安原小百合, 斎藤芳郎, 野口範子

生命科学系学会合同年次大会　2017年度　[3P-0672]　2017/12
Publisher: 生命科学系学会合同年次大会運営事務局
必須微量元素"セレン"の生物学と医学-発見から200年を迎えて血漿セレン含有タンパク質セレノプロテインPの機能と疾患レドックスバランスと膵β細胞の機能

斎藤芳郎

生命科学系学会合同年次大会　2017年度　[4PW24-4]　2017/12
Publisher: 生命科学系学会合同年次大会運営事務局
ヒト皮膚細胞モデルHaCaTにおけるDJ-1誘導因子の同定および酸化ストレス防御効果の評価

安藤万由, 斎藤芳郎, 石渡潮路, 松熊祥子, 野口範子

生命科学系学会合同年次大会　2017年度　[4AT18-0506)]　2017/12
Publisher: 生命科学系学会合同年次大会運営事務局
P210型BCR‐ABL PHドメインのリガンド特性およびその病理的意義の解明

島崎健太朗, 高橋美帆, 梅田真郷, 舟本聡, 斎藤芳郎, 野口範子, 熊谷圭吾, 花田賢太郎, 塚原富士子, 丸義朗, 柴田識人, 内藤幹彦, 内藤幹彦, 西川喜代孝

日本生化学会大会(Web)　2017年度　[1PT26-0039)]　2017/12
Publisher: 生命科学系学会合同年次大会運営事務局
Decrease of Insulin Secretion is Induced by Excess Selenoprotein P-Improving Effects of Neutralizing Antibody

Yoshiro Saito, Yuichiro Mita, Kaho Nakayama, Shogo Inari, Takahiro Nagamura, Noriko Noguchi

FREE RADICAL BIOLOGY AND MEDICINE　112　156-156　2017/11

DOI： 10.1016/j.freeradbiomed.2017.10.239 　

ISSN： 0891-5849

eISSN： 1873-4596
Interleukin-27 Induces p47(phox) in Monocyte-derived Macrophages and Dendritic cells and Enhances the Potential of Reactive Oxygen Species Generation

Yoshiro Saito, Bharatwaj Sowrirajan, Deepak Poudyal, Noriko Noguchi, Harry L. Malech, H. Clifford Lane, Tomozumi Imamichi

FREE RADICAL BIOLOGY AND MEDICINE　112　210-210　2017/11

DOI： 10.1016/j.freeradbiomed.2017.10.334 　

ISSN： 0891-5849

eISSN： 1873-4596
ヒト血中ヘパトカインレベルの日内、摂食および75g糖負荷後の変動

毛利研祐, 御簾博文, 圓山泰史, 高山浩昭, 竹下有美枝, 斎藤芳郎, 篁俊成

糖尿病　60　(Suppl.1)　S-159　2017/04
Publisher: (一社)日本糖尿病学会
ISSN： 0021-437X

eISSN： 1881-588X
エイコサペンタエン酸内服が2型糖尿病患者のインスリン感受性と血中セレノプロテインP濃度に及ぼす効果

寺村千里, 御簾博文, 高山浩昭, 斎藤芳郎, 井川寛章, 木谷佐央理, 中川浩実, 田中健雄, 島孝佑, 竹下有美枝, 篁俊成

糖尿病　60　(Suppl.1)　S-238　2017/04
Publisher: (一社)日本糖尿病学会
ISSN： 0021-437X

eISSN： 1881-588X
メトホルミンの治療効果を予知する新規バイオマーカーとしてのセレノプロテインPの可能性

金森岳広, 御簾博文, 田中睦, 斉藤芳郎, 齋藤麗奈, 毛利研祐, 竹下有美枝, 篁俊成

糖尿病　59　(Suppl.1)　S-139　2016/04
Publisher: (一社)日本糖尿病学会
ISSN： 0021-437X

eISSN： 1881-588X
ヒト血中ヘパトカインレベルの日内、摂食後および75g糖負荷後の変動

毛利研祐, 御簾博文, 高山浩昭, 竹下有美枝, 田中睦, 斎藤芳郎, 篁俊成

糖尿病　59　(Suppl.1)　S-140　2016/04
Publisher: (一社)日本糖尿病学会
ISSN： 0021-437X

eISSN： 1881-588X
セレノプロテインPの阻害抗体による糖尿病治療効果の解析インスリン抵抗性および分泌能を改善する抗体医薬の開発

三田雄一郎, 中山華穂, 稲荷尚吾, 西藤有希奈, 吉岡佑弥, 曽谷奏, 高部稚子, 御簾博文, 篁俊成, 高橋和彦, 野口範子, 斎藤芳郎

糖尿病　59　(Suppl.1)　S-444　2016/04
Publisher: (一社)日本糖尿病学会
ISSN： 0021-437X
Selenoprotein Pの中和抗体による耐糖能異常及びインスリン分泌能の改善

三田雄一郎, 三田雄一郎, 中山華穂, 稲荷尚吾, 吉岡佑弥, 高部稚子, 御簾博文, 篁俊成, 野口範子, 斎藤芳郎

日本酸化ストレス学会学術集会プログラム・抄録集　69th　2016
セレノプロテインPの阻害抗体による糖尿病治療効果の解析-インスリン抵抗性および分泌能を改善する抗体医薬の開発

三田雄一郎, 中山華穂, 稲荷尚吾, 西藤有希奈, 吉岡佑弥, 曽谷奏, 高部稚子, 御簾博文, 篁俊成, 高橋和彦, 野口範子, 斎藤芳郎

糖尿病(Web)　59　(Suppl)　2016

ISSN： 1881-588X
Biology of selenium : molecular function of selenoproteins and related diseases

斎藤芳郎

細胞工学 = Cell technology　35　(3)　240-246　2016
Publisher: 学研メディカル秀潤社 ; 1982-2016
ISSN： 0287-3796
膵臓β細胞モデルMIN6は過剰なSelenoprotein Pにより障害を受ける

稲荷尚吾, 高部稚子, 三田雄一郎, 御簾博文, 篁俊成, 野口範子, 斎藤芳郎

日本生化学会大会・日本分子生物学会年会合同大会講演要旨集　88回・38回　[4T特L-10(3P1201)]　2015/12
Publisher: (公社)日本生化学会
SBP2変異によるセレン含有タンパク質欠乏患者におけるコレステロールの酸化-細胞膜と血漿リポタンパク質の酸化反応の違い

齋藤芳郎, 七里元督, 濱島崇, 萩原義久, 吉田康一, 野口範子

脂質生化学研究　57　146-149　2015/05
Publisher: 日本脂質生化学会
ISSN： 0285-1520
ヘパトカインセレノプロテインP血中濃度測定によるメトホルミンの治療効果予知

毛利研祐, 御簾博文, 田中睦, 斎藤芳郎, 竹下有美枝, 斎藤麗奈, 金森岳広, 金子周一, 篁俊成

糖尿病　58　(Suppl.1)　S-271　2015/04
Publisher: (一社)日本糖尿病学会
ISSN： 0021-437X

eISSN： 1881-588X
ヘパトカインセレノプロテインP血中濃度による運動療法抵抗性の予知に関する検討

御簾博文, 田中睦, 斎藤芳郎, 石井清朗, 竹下有美枝, 金森岳広, 赤澤暢彦, 前田清司, 竹越一博, 金子周一, 篁俊成

糖尿病　58　(Suppl.1)　S-390　2015/04
Publisher: (一社)日本糖尿病学会
ISSN： 0021-437X

eISSN： 1881-588X
2型糖尿病患者におけるメトホルミンの血糖低下能に関するヘパトカインセレンタンパク質Pの血中濃度による予測(Blood levels of hepatokine selenoprotein P predict glucose-lowering effects of metformin in patients with type 2 diabetes)

Mohri Kensuke, Misu Hirofumi, Tanaka Mutsumi, Saito Yoshiro, Takeshita Yumie, Kanamori Takehiro, Saito Reina, Kaneko Shuichi, Takamura Toshinari

糖尿病　58　(Suppl.1)　S-472　2015/04
Publisher: (一社)日本糖尿病学会
ISSN： 0021-437X
Novel Method for Suppression of Neuronal Cell Death by 24S-Hydroxycholesterol

55　(4)　59-62　2015/01
Publisher: 同志社大学理工学研究所
ISSN： 0036-8172
1-I-11 血漿セレン含有タンパク質セレノプロテインPを標的とした2型糖尿病の抗体医薬の開発(一般演題要旨,ビタミン・バイオファクター研究のさらなる魅力～大和まほろぱからの発信～,第67回大会講演要旨)

斎藤芳郎, 中山華穂, 三田雄一郎, 野口範子

ビタミン　89　(4)　214-214　2015
Publisher: 公益社団法人日本ビタミン学会
ISSN： 0006-386X
Identification of neuron-derived protecting factors against oxidative stress

野口範子, 斎藤芳郎

コスメトロジー研究報告　23　61-64　2015
Publisher: コスメトロジー研究振興財団
ISSN： 2188-563X
Enhancement of Oxidative Stress and Its Amelioration by Vitamin E in a Subject with Mutations in the Selenocysteine Insertion Sequence-Binding Protein 2 (SBP2) Gene

Yoshiro Saito, Mototada Shichiri, Takashi Hamajima, Noriko Noguchi

FREE RADICAL BIOLOGY AND MEDICINE　76　S90-S90　2014/11

DOI： 10.1016/j.freeradbiomed.2014.10.314 　

ISSN： 0891-5849

eISSN： 1873-4596
血中oxDJ-1の異常高値を示し、幻覚を認めたPDの4例

西郷和真, 斎藤芳郎, 小川郁子, 細井幸恵, 三井良之, 花田一志, 上田昌美, 石井一成, 野口範子, 楠進

Dementia Japan　28　(4)　504-504　2014/10
Publisher: (一社)日本認知症学会
ISSN： 1342-646X
血中酸化型DJ‐1異常高値の臨床的意義

西郷和真, 斎藤芳郎, 小川郁子, 細井幸恵, 三井良之, 花田一志, 上田昌美, 石井一成, 野口範子, 楠進

日本酸化ストレス学会学術集会プログラム・抄録集　67th　52　2014/08/29
セレンタンパク質研究の最前線血漿セレノプロテインPによるセレン代謝制御と2型糖尿病

斎藤芳郎, 吉岡佑弥, 三田雄一郎, 御簾博文, 田中睦, 篁俊成, 野口範子

Biomedical Research on Trace Elements　25　(2)　50-50　2014/06
Publisher: 日本微量元素学会
ISSN： 0916-717X
脂肪肝患者におけるヘパトカインセレノプロテインP血中濃度と臓器別インスリン感受性の関連

加藤健一郎, 御簾博文, 田中睦, 斎藤芳郎, 竹下有美枝, 金子周一, 篁俊成

糖尿病　57　(Suppl.1)　S-251　2014/04
Publisher: (一社)日本糖尿病学会
ISSN： 0021-437X

eISSN： 1881-588X
脳特異的オキシステロール24S-hydroxycholesterolによる細胞死メカニズムの解析

浦野泰臣, 山中一哲, 高部稚子, 斎藤芳郎, 野口範子

日本Cell Death学会学術集会プログラム抄録集　23rd　2014
酸化コレステロール24S-OHCにより誘導されるNecroptosisのメカニズム

高部稚子, 山中一哲, 浦野泰臣, 斎藤芳郎, 野口範子

日本酸化ストレス学会学術集会プログラム・抄録集　67th　2014
Investigation of Antioxidants Against Neuronal Cell Death Induced by Glutamate and Its Molecular Mechanisms

斎藤芳郎

同志社大学理工学研究報告　54　(4)　11-15　2014/01
Publisher: 同志社大学理工学研究所
ISSN： 0036-8172
Molecular Mechanisms of Neuronal Cell Death Induced by 24S-hydroxycholesterol

斎藤芳郎

同志社大学理工学研究報告　54　(4)　16-20　2014/01
Publisher: 同志社大学理工学研究所
ISSN： 0036-8172
Study on Involvement of Reactive Oxygen Species in Neuronal Cell Death Induced by Oxidation Product of Cholesterol

野口範子, 斎藤芳郎, 浦野泰臣

同志社大学理工学研究報告　54　(4)　21-25　2014/01
Publisher: 同志社大学理工学研究所
ISSN： 0036-8172
Circulating levels of selenoprotein P predict future hyperglycaemia in non-diabetic Japanese people

H. Misu, T. Kanamori, Y. Takeshita, Y. Saito, M. Tanaka, S. Kaneko, T. Takamura

DIABETOLOGIA　56　S182-S182　2013/09

ISSN： 0012-186X

eISSN： 1432-0428
脳特異的24(S)-ヒドロキシコレステロールにより誘導されるプログラムネクローシスおよび細胞保護作用の分子メカニズム

斎藤芳郎, 山中一哲, 浦野泰臣, 野口範子

脂質生化学研究　55　9-9　2013/05/28

ISSN： 0285-1520
インスリン抵抗性誘導ヘパトカインセレノプロテインPによる高血糖発症予知に関する検討

御簾博文, 田中睦, 斎藤芳郎, 竹下有美枝, 喜多裕樹, 中源雅俊, 長野亨, 金子周一, 篁俊成

糖尿病　56　(Suppl.1)　S-118　2013/04
Publisher: (一社)日本糖尿病学会
ISSN： 0021-437X

eISSN： 1881-588X
Novel insights of brain-specific produced oxysterol in neurodegenerative diseases

NOGUCHI Noriko, YAMANAKA Kazunori, TAKABE Wakako, URANO Yasuomi, SAITO Yoshiro

日本生化学会大会(Web)　86th　2013
パーキンソン病におけるバイオマーカーの現状—マイケルＪフォックス財団の取り組み

斎藤芳郎

ファルマシア　49　(9)　870-872　2013
Publisher: 公益社団法人日本薬学会
DOI： 10.14894/faruawpsj.49.9_870 　

ISSN： 0014-8601
2-IV-13 セレン欠乏に伴う酸化ストレス障害に対するビタミンEの効果 : SBP2遺伝子異常に対する治療への応用(一般演題要旨,第65回大会講演要旨)

斎藤芳郎, 七里元督, 濱島崇, 萩原義久, 吉田康一, 野口範子

ビタミン　87　(4)　2013
Publisher: 公益社団法人日本ビタミン学会
ISSN： 0006-386X
パーキンソン病における酸化型DJ-1測定とMIBG心筋シンチグラフィーの関連について

西郷和真, 斎藤芳郎, 池上郁子, 細井幸子, 高田和男, 宮本勝一, 三井良之, 楠進, 野口範子

臨床神経学　52　(12)　1428-1428　2012/12
Publisher: (一社)日本神経学会
ISSN： 0009-918X

eISSN： 1882-0654
G020021 Reduction of Vitamin E radical in Electron-beam-irradiated dl-α-Tocopherol-blended Ultra High Molecular Weight Polyethylene

Iwade H, Kawasaki T, Tajima K, Sakurai Y, Noguchi N, Saito Y, Uetsuki K, Tomita N

Mechanical Engineering Congress, Japan　2012　"G020021-1"-"G020021-4"　2012/09/09
Publisher: The Japan Society of Mechanical Engineers

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Electron-beam irradiated Vitamin E-blended Ultra-High Molecular Weight Polyehylene (UHMWPE) has been studied as a bearing material for use in hip prosthesis. Although radiation crosslinking has been successful in decreasing wear volume, Vitamin E radicals are formed during radiation crosslinking of Vitamin E-blended UHMWPE and it is hypothesized that these Vitamin E radicals may negatively impact the materials biological activity In this study, ascorbic acid 6-palmitate (lipophilic vitamin C) was applied to electron-beam-irradiated Vitamin E-blended UHMWPE in an attempt to reduce the Vitamin E radicals UHMWPE resin powder was mixed with Vitamin E at 0.3 wt% and molded under direct compression at 25MPa and 220℃ Cylindrical pins (length: 40mm, diameter: 3.5mm) were then machined from these bulk samples, packaged in a vacuum, and irradiated by electron-beam at 300kGy. Samples were subsequently doped with either ascorbic acid 6-palmitate or ethanol and subjected to a hydrostatic pressure of 100MPa for 7, 14, and 21 days at room temperature. Electron Spin Resonance (ESR) was used to measure the radicals in samples. The observed characteristic ESR peak for Vitamin E radicals was shown to decrease with time in the electron-beam-irradiated Vitamin E-blended UHMWPE samples that were doped with ascorbic acid 6-palmitate While due to the fact that Vitamin E radicals in UHMWPE have been shown to be stable at room temperature, it is thought that the observed reduction in number of VE radicals is a result of the direct action ascorbic acid 6-palmitate.
レドックス制御研究の最先端抗酸化ヘパトカインセレノプロテインPによる運動療法抵抗性の発症

御簾博文, 篁俊成, 斎藤芳郎, 高橋和彦, 金子周一

日本薬学会年会要旨集　132年会　(1)　107-107　2012/03
Publisher: (公社)日本薬学会
ISSN： 0918-9823
トコフェロール・トコトリエノールによる抗酸化作用を介した神経保護効果

斎藤芳郎, 二木悦雄, 野口範子

ビタミンE研究の進歩　15　73-79　2012
早期パーキンソン病患者の赤血球におけるDJ‐1の酸化

斎藤芳郎, 浜窪隆雄, 下濱俊, 二木鋭雄, 野口範子

日本酸化ストレス学会学術集会プログラム・抄録集　64th　60　2011/06/27
パーキンソン病における新たなバイオマーカーとしての酸化型DJ‐1測定の可能性

西郷和真, 斎藤芳郎, 三井良之, 楠進, 野口範子

パーキンソン病・運動障害疾患コングレスプログラム・抄録集　5th　92　2011
Correlation between saliva cortisol concentration and sympathovagal balance before sleep in young male subjects.

Yoshino Kohzoh, Saito Yoshiro, Jitousyo Mamiko, Yoshida Yasukazu

Stress Science Research　26　48-52　2011
Publisher: 公益財団法人パブリックヘルスリサーチセンター
DOI： 10.5058/stresskagakukenkyu.26.48 　

ISSN： 1341-9986

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The aim of this study is to investigate the correlation between saliva cortisol concentration and balance of autonomic nervous system (sympathovagal balance) before sleep in normal male subjects. The subjects (N=27) intermittently wore an ambulatory wearable device that records heart rate variability (RR-interval) for three days during daily life. Their saliva was sampled at each night before sleep. The cortisol concentration of each sample was quantified. The sympathovagal balance was evaluated by calculating the normalized high-frequency power (HFnu) of RR-interval variability that was measured from A+5 to A minutes (A=0, 5,..., 55) before the saliva sampling time. The correlation coefficients between high values of saliva cortisol concentration and the corresponding natural logarithm of HFnu were from -0.40 to -0.49 (p=0.006-0.034) when the values of A were 10, 15, 20, and 25. This result implies that hypothalamic-pituitary-adrenal (HPA) axis activity before sleep is significantly correlated with dominance of sympathetic nervous system activity with time lag of 10-30 minutes during relatively high stress condition.<br>
Significance of translocation of coenzyme Q10 to mitochondria in its whitening and anti-aging effects

斎藤芳郎

Cosmetology　19　66-69　2011
Publisher: コスメトロジー研究振興財団
脂質酸化物により誘導される適応反応のメカニズム

斎藤芳郎

放射線生物研究　45　(2)　160-169　2010/06
Publisher: 放射線生物研究会
ISSN： 0441-747X
新規糖尿病関連ヘパトカインセレノプロテインPの血管新生抑制作用に関する検討

御簾博文, 石倉和秀, 熊崎雅史, 林寛人, 山田賢裕, 高倉伸幸, 斎藤芳郎, 高橋和彦, 金子周一, 篁俊成

糖尿病　53　(Suppl.1)　S-95　2010/04
Publisher: (一社)日本糖尿病学会
ISSN： 0021-437X
24(S)-Hydroxycholesterol Induces SH-SY5Y Cell Death via Necroptosis, Programmed Necrosis

Kazunori Yamanaka, Yoshiro Saito, Tohru Yamamori, Yasuomi Urano, Noriko Noguchi

FREE RADICAL BIOLOGY AND MEDICINE　49　S137-S137　2010

DOI： 10.1016/j.freeradbiomed.2010.10.382 　

ISSN： 0891-5849
Cytoprotective Effect of Vitamin E Homologues Against Glutamate-induced Cell Death in Immature Primary Cortical Neuron Cultures: Tocopherols and Tocotrienols Exert Similar Effects by Antioxidant Function

Yoshiro Saito, Yasukazu Yoshida, Noriko Noguchi, Etsuo Niki

FREE RADICAL BIOLOGY AND MEDICINE　49　S196-S196　2010

DOI： 10.1016/j.freeradbiomed.2010.10.567 　

ISSN： 0891-5849
Elevation of Oxidized DJ-1 in the Erythrocytes of Parkinson Disease Patients and Animal Models

Yoshiro Saito, Yoko O. Akazawa, Takao Hamakuho, Yasukazu Yoshida, Noriko Noguchi, Etsuo Niki

FREE RADICAL BIOLOGY AND MEDICINE　49　S171-S171　2010

DOI： 10.1016/j.freeradbiomed.2010.10.485 　

ISSN： 0891-5849
グルタミン酸誘導性の神経細胞死に対するビタミンE類の抑制効果

斎藤芳郎, 西尾敬子, 赤澤(小川)陽子, 吉田康一, 野口範子, 二木鋭雄

ビタミンE研究の進歩　14　27-32　2010
3.24(S)-HyDroxycholesterolによる神経細胞死の誘導メカニズム(第327回会議研究発表要旨,脂溶性ビタミン総合研究委員会)

野口範子, 山中哲一, 斉藤芳郎, 浦野泰臣

ビタミン　84　(9)　448-448　2010
Publisher: 公益社団法人日本ビタミン学会
DOI： 10.20632/vso.84.9_448 　

ISSN： 0006-386X
翻訳されうる21番目のアミノ酸、セレノシステインを含有するタンパク質研究のブレーク・スルー新規インスリン抵抗性誘導ヘパトカインセレノプロテインPの同定セレン含有タンパクによる糖代謝悪化の可能性

御簾博文, 高山浩昭, 林寛人, 斎藤芳郎, 高橋和彦, 篁俊成

日本生化学会大会プログラム・講演要旨集　82回　2S8a-5　2009/09
Publisher: (公社)日本生化学会
24S-hydroxycholesterol による神経細胞傷害メカニズムの解析

山中一哲, 斎藤芳郎, 山盛徹, 浦野泰臣, 野口範子

脂質生化学研究　51　69-72　2009/07/10

ISSN： 0285-1520
新規ヘパトカインセレノプロテインPを介した肝臓-脂肪組織ネットワーク

石倉和秀, 御簾博文, 杉森慎, 磯部優希, 清水暁子, 栗田征一郎, 竹下有美枝, 斎藤芳郎, 高橋和彦, 金子周一, 篁俊成

糖尿病　52　(Suppl.1)　S-161　2009/04
Publisher: (一社)日本糖尿病学会
ISSN： 0021-437X

eISSN： 1881-588X
酸化DJ-1とパーキンソン病(1):抗体作成とELISA開発

斎藤芳郎, 斎藤芳郎, 浜窪隆雄, 吉田康一, 小川陽子, 岩成宏子, 望月康弘, 七里元督, 西尾敬子, 絹見朋也, 野口範子, 児玉龍彦, 二木鋭雄

日本酸化ストレス学会学術集会プログラム・抄録集　62nd　2009
酸化DJ-1とパーキンソン病(2):臨床検体の測定

小川陽子, 斎藤芳郎, 浜窪隆雄, 児玉龍彦, 原保夫, 藤村晴俊, 今井康陽, 岩成宏子, 七里元督, 西尾敬子, 野口範子, 吉田康一, 二木鋭雄

日本酸化ストレス学会学術集会プログラム・抄録集　62nd　2009
Significant Elevation of Oxidized DJ-1 in Erythrocytes of Early-Stage Parkinson Disease Patients: Potential Application of Oxidized DJ-1 Levels for Diagnosis of PD at Early Stage

Yoshiro Saito, Takao Hamakuba, Yasukazu Yoshida, Yoko Ogawa Akazawa, Mototado Shichiri, Noriko Noguchi, Etsuo Niki

FREE RADICAL BIOLOGY AND MEDICINE　47　S80-S80　2009

ISSN： 0891-5849
血漿セレン含有蛋白質セレノプロテインPに関する最近の話題

斎藤芳郎

ビタミン　83　662-665　2009

DOI： 10.20632/vso.83.12_662 　
Recent topics about selenium-containing extracellular protein selenoprotein P

Saito Yoshiro

vitamins　83　(12)　662-665　2009
Publisher: 公益社団法人日本ビタミン学会
DOI： 10.20632/vso.83.12_662 　

ISSN： 0006-386X
2-III-19 γ-トコフェリルキノンは細胞内レドックスシグナルの亢進により適応応答を誘導する(一般研究発表,日本ビタミン学会第61回大会研究発表要旨)

小川陽子, 斎藤芳郎, 西尾敬子, 吉田康一, 二木鋭雄

ビタミン　83　(4)　217-217　2009
Publisher: 公益社団法人日本ビタミン学会
ISSN： 0006-386X
バイオマーカーとしての脂質酸化物

吉田康一, 今井康陽, 澤井良之, 吉川敦, 斎藤芳郎, 早川三恵子, 羽渕洋子, 二木鋭雄

脂質生化学研究　50　21-21　2008/06/05

ISSN： 0285-1520
リポ多糖(LPS)により誘導される適応反応・酸化ストレス耐性メカニズムの解析

斎藤芳郎, 小俣葉, 藤田克英, 吉田康一, 野口範子, 二木鋭雄

生化学　4P-0442　2008

ISSN： 0037-1017
ストレスに対する生体の応答蛋白質

斎藤芳郎

ストレスの科学と健康　52-59　2007
2-IV-15 トコフェリルキノンにより誘導される酸化ストレス耐性の応答メカニズム(ビタミン学の原点・栄養学への21世紀的回帰, 日本ビタミン学会第59回大会)

小川陽子, 斎藤芳郎, 西尾敬子, 吉田康一, 二木鋭雄

ビタミン　81　(4)　186-186　2007
Publisher: 公益社団法人日本ビタミン学会
ISSN： 0006-386X
Antioxidant Function of essential trace element "selenium"

SAITO Yoshiro

バイオサイエンスとインダストリー = Bioscience & industry　64　(64)　159-160　2006/03/01

ISSN： 0914-8981
Molecular mechanisms of 6-hydroxydopamine-induced neurotoxicity

Yoshiro Saito, Keiko Nishio, Yoko Ogawa, Tomoya Kinumi, Yasukazu Yoshida, Yoshinori Masuo, Etsuo Niki

FREE RADICAL BIOLOGY AND MEDICINE　41　S168-S168　2006

ISSN： 0891-5849
Environmental stress and apoptosis

Yoshinori Mastro, Yoshiro Saito, Yasukazu Yoshida, Etsuo Niki

NEUROSCIENCE RESEARCH　55　S40-S40　2006

ISSN： 0168-0102
抗酸化蛋白質DJ-1の酸化修飾による機能制御

斎藤芳郎

蛋白質の翻訳後修飾と疾患プロテオミクス　34-40　2006
A turning point to apoptotic and necrotic cell death induced by hydrogen peroxide

Y Saito, K Nishio, Y Ogawa, T Kinumi, Y Yoshida, N Noguchi, E Niki

FREE RADICAL BIOLOGY AND MEDICINE　39　S147-S147　2005

ISSN： 0891-5849
4-hydroxynonenal induces adaptive response and enhances PC12 cell tolerance primarily through induction of thioredoxin reductase 1 via activation of NRF2

ZH Chen, Y Saito, Y Yoshida, A Sekine, N Noguchi, E Niki

FREE RADICAL BIOLOGY AND MEDICINE　39　S69-S69　2005

ISSN： 0891-5849
必須微量元素セレン及び酸化ストレスに伴う細胞死に対するAOBの添加効果

斎藤芳郎

AOB研究会　(4)　42-46　2005
WS-9-07 gemcitabine耐性膵癌に対する新規治療法の検討(ワークショップ9 : 分子生物・遺伝子研究の消化器癌補助療法への応用)

前原伸一郎, 島田光生, 調憲, 田中真二, 斎藤芳郎, 高橋和彦, 前原喜彦

日本消化器外科学会雑誌　37　(7)　1004-1004　2004/07/01
Publisher: 一般社団法人日本消化器外科学会
ISSN： 0386-9768
1-IV-3 ビタミンE同族体の眼球組織移行性に関する研究(第56回大会一般研究発表)

吉田康一, 戸谷正樹, 伊藤奈々子, 斎藤芳郎, 大平明弘, 二木悦雄

ビタミン　78　(4)　235-235　2004/04/25
Publisher: 日本ビタミン学会
ISSN： 0006-386X
Synergistic cytotoxic effects of formaldehyde and free radicals

Y Saito, K Nishio, Y Yoshida, E Niki

FREE RADICAL BIOLOGY AND MEDICINE　37　S144-S144　2004

ISSN： 0891-5849
Antioxidative effects of volatile constituents of a rosemary extract on the lipid oxidation and cell damage

A Shiga, Y Saito, T Furuhashi, J Hoshizaki, Y Fujita, Y Yoshida, E Niki

FREE RADICAL BIOLOGY AND MEDICINE　37　S43-S43　2004

ISSN： 0891-5849
Vitamin E and BO-653: Natural vs. synthetic antioxidant

E Niki, Y Yoshida, Y Saito, N Itoh, O Cynshi, N Noguchi, T Kodama

FREE RADICAL BIOLOGY AND MEDICINE　36　S7-S7　2004

ISSN： 0891-5849
トコトリエノールのストレス抑制作用と細胞内取り込みについて

斎藤芳郎

ビタミンE研究の進歩　(11)　108-114　2004
紫外線とNO2による酸化反応に対するローズマリー揮発成分の抑制効果

斎藤芳郎, 志賀彰, 吉田康一

Aroma research　5　(2)　118-122　2004
Publisher: フレグランスジャーナル社
ISSN： 1345-4722
Reduction of lipid hydroperoxides in oxidized LDL by extracellular glutathione peroxidase and selenoprotein P

G Takebe, K Takashima, Y Saito, T Hayashi, S Nagasawa, K Takahashi

ATHEROSCLEROSIS SUPPLEMENTS　4　(2)　286-286　2003/09

ISSN： 1567-5688
膵癌における抗癌剤(gemcitabine)耐性規定遺伝子の同定と感受性診断への応用

前原伸一郎, 田中真二, 島田光生, 調憲, 斎藤芳郎, 高橋和彦, 前原喜彦

日本消化器外科学会雑誌　36　(7)　871-871　2003/07/01
Publisher: 一般社団法人日本消化器外科学会
ISSN： 0386-9768
必須微量元素セレンの細胞生存維持作用に関する研究

斎藤芳郎, 吉田康一, 二木鋭雄, 高橋和彦

脂質生化学研究　45　262-265　2003/06/20

ISSN： 0285-1520
抗癌剤gemcitabine感受性規定遺伝子の網羅的解析による治療指標の同定

前原伸一郎, 島田光生, 調憲, 田中真二, 斎藤芳郎, 高橋和彦, 前原喜彦

日本外科学会雑誌　104　(0)　286-286　2003/04/30
Publisher: 一般社団法人日本外科学会
ISSN： 0301-4894
Antioxidant action of vitamin E isoforms

E Niki, Y Yoshida, Y Saito, R Piga, N Noguchi

FREE RADICAL RESEARCH　37　40-40　2003

ISSN： 1071-5762
Cell death caused by selenium deficiency and protective effect of antioxidants

Y Saito, Y Yoshida, K Takahashi, E Niki

FREE RADICAL BIOLOGY AND MEDICINE　35　S46-S46　2003

ISSN： 0891-5849
Reduction of hydroperoxides in oxLDL and inhibition of oxLDL formation by extracellular selenium-containing antioxidant enzymes

G Takebe, K Takashima, Y Saito, T Hayashi, K Takahashi

FREE RADICAL BIOLOGY AND MEDICINE　33　S145-S146　2002

ISSN： 0891-5849
Characterization of selenoprotein P as a selenium transport protein

Y Saito, E Niki, K Takahashi

FREE RADICAL BIOLOGY AND MEDICINE　33　S92-S92　2002

ISSN： 0891-5849
血漿セレン含有蛋白質Selenoprotein Pのユニークな構造とその機能

斎藤芳郎

放射線生物研究　36　(36)　291-301　2001/09
Publisher: 放射線生物研究会
ISSN： 0441-747X
Glutathione peroxidase family の酸化LDL産生に及ぼす影響

建部厳, 高嶋和巳, 斎藤芳郎, 高橋和彦, 林隆章

脂質生化学研究　43　311-313　2001/05/10

ISSN： 0285-1520
Structure and function of human selenoprotein P

TAKAHASHI Kazuhiko, SAITO Yoshiro

生化學　73　(73)　261-264　2001/04/25
Publisher: 日本生化学会
ISSN： 0037-1017
Structure and function of human selenoprotein P

K. Takahashi, Y. Saito

Seikagaku　73　(4)　261-264　2001

ISSN： 0037-1017
全く異なる２つの顔を持つ蛋白質

斎藤芳郎

ファルマシア　(36)　513-514　2000
全く異なる2つの顔を持つタンパク質

斎藤芳郎

ファルマシア　36　(6)　513-514　2000
Publisher: 公益社団法人日本薬学会
ISSN： 0014-8601
Selenoprotein P as an extracellular phospholipid hydroperoxide glutathione peroxidase

Y Saito, T Hayashi, A Tanaka, M Suzuki, E Saito, K Takahashi

FREE RADICAL BIOLOGY AND MEDICINE　25　S38-S38　1998

ISSN： 0891-5849
ヒト血漿セレン含有蛋白質SePの精製と構造解析

斎藤芳郎, 西村仁, 高橋和彦

日本分子生物学会年会プログラム・講演要旨集　19　490-490　1996/08/01

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Books and Other Publications 8

神経変性とレドックスーパーキンソン病関連分子DJ-1のレドックス制御機能レドックスUPDATE

医歯薬出版　2015
パーキンソン病と酸化ストレス酸化ストレスの医学第2版

診断と治療社　2014
グルタミン酸誘導性の神経細胞死に対するビタミンE類の抑制効果

ビタミンE研究の進歩　2010
Cytoprotective effects of vitamin E homologues against glutamate-induced neuronal cell death

Progress of vitamin E research　2010
A Gene Expression Profiling Approach to Study the Influence of Ultrafine Particles on Rat Lungs.

Atmospheric and Biological Environmental Monitoring　2009
A Gene Expression Profiling Approach to Study the Influence of Ultrafine Particles on Rat Lungs.

Atmospheric and Biological Environmental Monitoring　2009
Uptake, Distribution and Protective Action of Tocotrienols in Cultured Cells.

Tocotrienols : Vitamin E Beyond Tocopherols　2008
Uptake, Distribution and Protective Action of Tocotrienols in Cultured Cells.

Tocotrienols : Vitamin E Beyond Tocopherols　2008

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Presentations 2

Novel Method for Suppression of Neuronal Cell Death by 24S-Hydroxycholesterol

野口範子, 斎藤芳郎, 浦野泰臣

同志社大学理工学研究報告　2015/01
新規糖尿病バイオマーカーを標的とする２型糖尿病治療薬

イノベーション・ジャパン2013　2013

Industrial Property Rights 27

セレノプロテインPの発現抑制剤及びその利用

斎藤芳郎, 三田雄一郎, 野口範子, 内田理沙, 安原小百合, 横大路将, 白川静乃

Property Type: Patent
2型糖尿病患者の治療薬選択の補助方法、治療薬の効果予測方法、検査方法及び治療方法

御簾博文, 金子周一, 竹下有美枝, 篁俊成, 斎藤芳郎, 田中睦

Property Type: Patent
２型糖尿病の治療及び／又は予防薬

斎藤芳郎, 野口範子, 三田雄一郎, 中山華穂

Property Type: Patent

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特願2013-175612
細胞死抑制剤

浦野泰臣, 野口範子, 斎藤芳郎, 山中一哲

Property Type: Patent
細胞死抑制剤

浦野泰臣, 野口範子, 斎藤芳郎, 山中一哲

特許第6143435号

Property Type: Patent

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特願2012-242950
被測定物質の分別測定方法

田中睦, 斎藤芳郎

Property Type: Patent

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特願2012-198464
含硫アミノ酸残基を含むポリペプチドに対する抗体

斎藤芳郎, 野口範子, 浜窪隆雄, 岩成宏子, 二木鋭雄, 吉田康一, 新井修

Property Type: Patent
含硫アミノ酸残基を含むポリペプチドに対する抗体

斎藤芳郎, 野口範子, 浜窪隆雄, 岩成宏子, 二木鋭雄, 吉田康一, 新井修

特許第5885158号

Property Type: Patent

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特願2012-028138
過酸化脂質の測定方法

斎藤芳郎, 野口範子, 山中一哲, 崎▼山順次, 大瀬戸文夫

Property Type: Patent

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特願2011-260819
生体の抗酸化能測定方法

斎藤芳郎, 野口範子, 澤田浩隆

Property Type: Patent

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特願2011-181963
含硫アミノ酸残基が酸化された酸化型ポリペプチドに対する抗体

吉田康一, 斎藤芳郎, 小川陽子, 二木鋭雄, 七里元督, 浜窪隆雄, 望月康弘, 岩成宏子, 細見直樹

Property Type: Patent

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特願2009-028042
酸化傷害抑制剤

斎藤芳郎, 二木鋭雄, 吉田康一, 加藤久豊, 山口修平

Property Type: Patent

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特願2008-100401
ペルオキシレドキシン6(Prx6)に対するアプタマー

御園智子, ペンメッチャクマール, 斎藤芳郎, 吉田康一

Property Type: Patent
ペルオキシレドキシン6(Prx6)に対するアプタマー

御園智子, ペンメッチャクマール, 斎藤芳郎, 吉田康一

特許第5083892号

Property Type: Patent
HCV患者における瀉血治療の効果の検査方法

吉田康一, 斎藤芳郎, 二木鋭雄, 今井康陽, 澤井良之

特許第5177630号

Property Type: Patent
HCV患者における瀉血治療の効果の判定方法及び判定キット

吉田康一, 斎藤芳郎, 二木鋭雄, 今井康陽, 澤井良之

Property Type: Patent

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特願2007-252895
含硫アミノ酸残基が酸化された酸化型ポリペプチドの製造方法

斎藤芳郎, 絹見朋也, 西尾敬子, 小川陽子, 吉田康一, 二木鋭雄

Property Type: Patent
含硫アミノ酸残基が酸化された酸化型ポリペプチドの製造方法

斎藤芳郎, 絹見朋也, 西尾敬子, 小川陽子, 吉田康一, 二木鋭雄

特許第4779103号

Property Type: Patent

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特願2006-153039
ウイルス性肝疾患の診断方法及び診断キット

吉田康一, 斎藤芳郎, 二木鋭雄, 今井康陽, 澤井良之

Property Type: Patent
Ｃ型肝炎ウイルスに起因する慢性肝炎及び肝硬変の指標とするための方法及びキット

吉田康一, 斎藤芳郎, 二木鋭雄, 今井康陽, 澤井良之

特許第4569959号

Property Type: Patent

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特許第4569959号
ラジカルを含む殺菌性材料

斎藤芳郎, 吉田康一, 二木鋭雄, 民谷栄一, 羽柴智彦, 川村幸嗣

Property Type: Patent

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特願2004-126525
メタノール、エタノールまたはホルムアルデヒドに由来する活性種を含む処理ガスのインジケーター

吉田康一, 二木鋭雄, 斎藤芳郎, 民谷栄一, 羽柴智彦, 川村幸嗣

Property Type: Patent

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特願2003-349980
抗酸化剤放出装置および抗酸化剤放出方法

志賀彰, 古橋拓也, 藤田洋司, 牧野浩招, 鈴木聡, 斎藤芳郎, 吉田康一, 二木鋭雄

Property Type: Patent

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特願2003-345543
アスベストの除去装置

古賀基之, 斎藤芳郎

特許第2707276号

Property Type: Patent
２型糖尿病患者の治療薬選択の補助方法、治療薬の効果予測方法及び検査方法

Property Type: Patent

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特願2014-184499
ペルオキシレドキシン６(Prx6)タンパク質の検出方法

Property Type: Patent

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特願2008-006123
ウィルス性肝疾患の診断方法及び診断キット

Property Type: Patent

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特願2005-174962

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Research Projects 21

Global Exploration for Redox Supermolecules Evolving in Life Functions

Offer Organization: Japan Society for the Promotion of Science

System: Grants-in-Aid for Scientific Research

Category: Fund for the Promotion of Joint International Research (International Leading Research )

Institution: Tohoku University

2023/11/17 - 2030/03/31
Elucidation of the molecular pathology of chronic diseases and establishment of new treatment methods based on trace element research

Offer Organization: Japan Society for the Promotion of Science

System: Grants-in-Aid for Scientific Research

Category: Grant-in-Aid for Scientific Research (A)

Institution: Tohoku University

2024/04/01 - 2028/03/31
The regulation mechanism of oxidation and hypersulfidation in increase of effects of exercise for diabetes prevention

Offer Organization: JST

System: KAKENHI

Category: B

Institution: Doshisha University

2024/04 - 2027/03
Elucidation of the direct metabolic control mechanisms of producing cells by secreted proteins

Offer Organization: Japan Society for the Promotion of Science

System: Grants-in-Aid for Scientific Research

Category: Grant-in-Aid for Challenging Research (Exploratory)

Institution: Tohoku University

2024/06/28 - 2026/03/31
Regulation of signal transduction via crosstalk between supersulfide and selenium

Offer Organization: Japan Society for the Promotion of Science

System: Grants-in-Aid for Scientific Research

Category: Grant-in-Aid for Transformative Research Areas (A)

Institution: Tohoku University

2021/09/10 - 2026/03/31
Management of international relation and facility for promotion of research on sulfur biology

Offer Organization: Japan Society for the Promotion of Science

System: Grants-in-Aid for Scientific Research

Category: Grant-in-Aid for Transformative Research Areas (A)

Institution: Tohoku University

2021/09/10 - 2026/03/31
The Blood Diagnostic Markers in Dementia with Lewy Bodies

Offer Organization: Japan Society for the Promotion of Science

System: Grants-in-Aid for Scientific Research

Category: Grant-in-Aid for Scientific Research (C)

Institution: Kindai University

2022/04/01 - 2025/03/31
Regulatory mechanism of selenoprotein P expression and its deterioration mechanism of glucose metabolism

Offer Organization: Japan Society for the Promotion of Science

System: Grants-in-Aid for Scientific Research Grant-in-Aid for Scientific Research (A)

Category: Grant-in-Aid for Scientific Research (A)

Institution: Tohoku University

2020/04/01 - 2024/03/31
Creation of "disease metallomics" to understand the relationship between fluctuations of heavy metals/trace elements and diseases

Offer Organization: Japan Society for the Promotion of Science

System: Grants-in-Aid for Scientific Research

Category: Grant-in-Aid for Challenging Research (Exploratory)

Institution: Tohoku University

2021/07/09 - 2023/03/31
Elucidation of a dynamics control mechanism of selenium

Offer Organization: Japan Society for the Promotion of Science

System: Grants-in-Aid for Scientific Research Grant-in-Aid for Scientific Research on Innovative Areas (Research in a proposed research area)

Category: Grant-in-Aid for Scientific Research on Innovative Areas (Research in a proposed research area)

Institution: Tohoku University

2020/04/01 - 2022/03/31
Fatigue assessment and analysis of trace element deficiency and eating habits survey for prevention of mental health disorder of university students

Offer Organization: Japan Society for the Promotion of Science

System: Grants-in-Aid for Scientific Research Grant-in-Aid for Scientific Research (C)

Category: Grant-in-Aid for Scientific Research (C)

Institution: Koshien University

2019/04/01 - 2022/03/31
Omics analysis for the establishment of "reductive stress," a biological disorder caused by excessive antioxidant and reductive environment

Saito Yoshiro

Offer Organization: Japan Society for the Promotion of Science

System: Grants-in-Aid for Scientific Research Grant-in-Aid for Challenging Research (Exploratory)

Category: Grant-in-Aid for Challenging Research (Exploratory)

Institution: Tohoku University

2019/06/28 - 2021/03/31

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Antioxidant systems that reduce and detoxify reactive oxygen species (ROS) play an important role in maintaining cell homeostasis. However, in recent years, biological disorders induced by excessive antioxidants and reducing enzymes, namely reductive stress, have caused insulin resistance, involving in the onset and progression of type 2 diabetes. Thus, the purpose of this study is to identify the characteristic cellular response in the excessive reduction state by the comprehensive analysis and to clarify the reductive stress response at the molecular level.
Molecular mechanisms of disorder of pancreatic beta cells induced by excess selenoprotein P

Saito Yoshiro

Offer Organization: Japan Society for the Promotion of Science

System: Grants-in-Aid for Scientific Research Grant-in-Aid for Scientific Research (B)

Category: Grant-in-Aid for Scientific Research (B)

Institution: Tohoku University

2017/04/01 - 2020/03/31

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Selenoprotein P (SeP), a plasma protein containing essential trace element selenium, functions as a transporter of selenium, delivering selenium to the cells. We found the increase of SeP levels in type 2 diabetes patients and have reported that increased SeP (excess SeP) worsen glucose metabolism via the increase of insulin resistance in the skeletal muscle and liver. In the present study, we found that excess SeP is incorporated into the pancreatic beta cells via SeP receptors and decreases insulin secretion via ER stress. Furthermore, we found the physiological role of SeP expression in the pancreatic beta cells and stated the novel metabolism regulation between the pancreas and liver via insulin and SeP.
Mechanism of inhibition of oxysterol-induced Alzheimer's disease by vitamin E

Noguchi Noriko

Offer Organization: Japan Society for the Promotion of Science

System: Grants-in-Aid for Scientific Research Grant-in-Aid for Scientific Research (C)

Category: Grant-in-Aid for Scientific Research (C)

Institution: Doshisha University

2016/04/01 - 2019/03/31

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While 24(S)-hydroxycholesterol（24S-OHC）plays an important role in cholesterol metabolism in the brain, its contribution in pathogenesis of Alzheimer’s disease (AD) has received attention. 24S-OHC was esterified by action of the enzyme at endoplasmic reticulum (ER) and caused formation of lipid droplet-like structure and disruption of ER membrane integrity, resulting in release of ER chaperones into cytosol. Vitamin homologues are divided into two group, tocotrienol (Toc3) and tocopherol (Toc), with and without double bonds at their side chain. The chaperone release and cell death induced by 24S-OHC were inhibited by Toc but not by Toc3. The critical effect of the side chain of vitamin E on ER membrane integrity and 24S-OHC-induced cell death was indicated.
Selenium-transport mechanism of selenoprotein P

Saito Yoshiro, NOGUCHI Noriko, TAKAHASHI Kazuhiko

Offer Organization: Japan Society for the Promotion of Science

System: Grants-in-Aid for Scientific Research Grant-in-Aid for Scientific Research (B)

Category: Grant-in-Aid for Scientific Research (B)

Institution: Doshisha University

2013/04/01 - 2017/03/31

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Selenoprotein P (SeP) is plasma selenoprotein containing essential trace element selenium. SeP functions as a transporter of selenium, delivering selenium to the cells. However, details of selenium-transport mechanisms of SeP remain unknown. In the present study, we identified SeP receptors in several tissues such as skeletal muscle, pancreas, and lymphocytes. Further, we identified SeP receptors with different affinity for SeP, and found a different molecular pathway to transport selenium of SeP to the cells. Collectively, we revealed selenium-transport mechanisms of SeP.
Development of diagnosis and treatment of Parkinson disease at early stage using novel biomarker oxidized DJ-1

Yoshiro Saito, NOGUCHI Noriko, SAIGOH Kazumasa

Offer Organization: Japan Society for the Promotion of Science

System: Grants-in-Aid for Scientific Research Grant-in-Aid for Challenging Exploratory Research

Category: Grant-in-Aid for Challenging Exploratory Research

Institution: Doshisha University

2013/04/01 - 2016/03/31

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DJ-1, the product of the causative gene of a familial form of Parkinson’s disease (PD), undergoes preferential oxidation at the cysteine residue at position 106 (Cys-106) under oxidative stress. In the present study using specific antibodies against Cys-106-oxidized DJ-1 (oxDJ-1), we evaluated oxDJ-1 levels in brain and blood of PD patients. It was found that DJ-1 oxidation in erythrocytes and in the brain occurs in PD patients, particularly during the early phases. DJ-1 oxidation was effectively inhibited by endogenous antioxidant glutathione. We could develop the molecular base for the diagnosis and treatment of PD at early phases based on the levels of oxDJ-1.
The study on functional food using oxidative stress marker, hydroxyoctadecadienoic acid and 7-hydroxycholesterol

YOSHIDA Yasukazu, NIKI Etsuo, AKAZAWA Yoko, SAITO Yoshiro

Offer Organization: Japan Society for the Promotion of Science

System: Grants-in-Aid for Scientific Research Grant-in-Aid for Scientific Research (B)

Category: Grant-in-Aid for Scientific Research (B)

Institution: National Institute of Advanced Industrial Science and Technology

2007 - 2009

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Lipid peroxidation products have received a great deal of attention for the partical application to clinical use as bio-markers. To assess the antioxidative role of functional foods and antioxidants, vitamin E and BO-653, in a mouse model and culture cell using lipid peroxidation and protein oxidation products. In the present study, we proposed that lipid peroxidation (tHODE and tOHCh) and protein oxidation are indeed good markers for the detection of progression of oxidative stress and effect of functional foods.
培養神経細胞および幼若ラット脳を用いたドーパミン神経障害メカニズムの探究

斎藤芳郎

Offer Organization: 日本学術振興会

System: 科学研究費助成事業若手研究(B)

Category: 若手研究(B)

Institution: 独立行政法人産業技術総合研究所

2006 - 2007

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本研究の目的は,6ーヒドロシドーパミン1-methy1-4-pheny-1,2,3,6-tetrahydropyridine(MPTP)など汎用されているドーパミン神経毒の作用について,ガン細胞,初代培養細胞および幼若ラット洋悩を用いて,in vitroおよびin vivoでの角析を同時に行い,その細胞障害メカニズムを明らかにすることにある。今年度は,ガン細胞である12細胞だけでなく,初代神経細胞においても15d-PGJ2や4-HNEなどの細胞毒性をもつアルデヒドが,神経細胞の適応応答を介して,6-OHDAやグルタミン酸による神経細胞死を抑制することを明らかにした(J Neurochemistry,102,1625-1634)。さらに,アリル化しうるキノンであるγ-トコフェリルキノンが,同様にガン細胞・初代神経細胞ともに適応反応を誘導することがわかった(現在投稿中)。これらは,細胞内のGSHを増加して、適応反応を誘導することがわかった。アルデヒド類はNrf2依存的に、グルタミン酸システインリガーゼの修飾サブユニットを誘導して,グルタチオンを誘導した。一方,γ-トコフェリキノンは,シスチンの取り込みを担うxCT,ATF4依存的に誘導することが明らかとなった。これらの適応反応およびGSHの増加は,各転写因子に対するsiRNA処理で,低下あるいは消失した。これらの適応反応に関する知見は,神経変性疾患の発症や進展に関与する可能性が考えられ,新たな創薬のヒントをいだす知見である。さらに,p-キノンにより誘導される神経細胞死メカニズムについては幼若ラット脳のプロテオーム解析からp-キノンで特異的に変化する分子を見いだしている。これらを同定し,初代培養系および幼若ラットで比較検討中である。
酸化血清中に存在する細胞傷害因子の探索-新規酸化ストレスマーカーの同定を目指して

斎藤芳郎

Offer Organization: 日本学術振興会

System: 科学研究費助成事業若手研究(B)

Category: 若手研究(B)

Institution: 独立行政法人産業技術総合研究所

2004 - 2005

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1.酸化血清中の血管細胞増殖因子の同定前年度の結果から、酸化血清中に含まれる過酸化脂質が主要な血管細胞増殖因子として機能する可能性が考えられた。このことを証明するため、脂質を除去した血清(Lipoprotein Deficient Serum以下LPDS)を作成し検討した。ヒト血清にKBrを加え、超遠心を行い、上層にリポタンパク質画分を、下層にLPDS画分を得た。透析して得られたLPDSをラジカル酸化剤を用いて酸化し、酸化LPDSを作成し、AKTAクロマトグラフィーを用いてゲルろ過で分離した。分離したフラクションを、前年度確立したバイオアッセイ系で評価した。48穴プレートに、ヒト動脈内皮細胞(HAEC)やヒト動脈平滑筋細胞(AoSMC)などのヒト由来血管細胞を播種し、分離したフラクションをくわえた。各画分を添加して、24〜72時間培養後、生細胞数をMTT法を用いて測定した。その結果、高分子画分に認められた増殖因子が消失した。さらに、低比重リポタンパク質(LDL)を同様に酸化し、得られた酸化LDLを血管細胞に添加した結果、類似の細胞増殖が認められた。以上の結果から、酸化血清中の主要な細胞増殖因子は、酸化LDLに由来することがわかった。酸化ストレスと動脈硬化との関係において、重要な知見が得られた。酸化LDLの測定系に関しは、当ヒューマンストレスシグナル研究センターの酸化脂質ストレスマーカーtHODE、t7-OHChとの相関性について検討を行っている。また、これまで我々の研究室で認められた酸化LDL添加により当電点が変化するタンパク質の解析を行っている。 2.接着分子の発現に及ぼす影響さらに、酸化血清の作用について、細胞表面への接着分子の発現に及ぼす影響について解析した。方法は同一で、得られた酸化血清フラクションを血管細胞に添加後、フローサイトメーターを用いて接着分子の発現量を定量した。その結果、生細胞数への影響とは異なるとこにピークが認められた。今後、この分子の同定を行っていきたい。
血漿セレン含有タンパク質セレノプロテインPの機能と生理的意義の解析

斎藤芳郎

Offer Organization: 日本学術振興会

System: 科学研究費助成事業特別研究員奨励費

Category: 特別研究員奨励費

Institution: 北海道大学

2000 - 2001
活性酸素種による適応反応のメカニズム Competitive

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Social Activities 9

東北大学学友会アメフト部ホーネッツ部長

2022/04/01 - Present
レドックスウィークイン仙台 2025 一般公開講座

2025/04/20 - 2025/04/20
フォーラム2024 衛生薬学・環境トキシコロジー若手研究者の会若手研究者のための勉強会「科研費申請書の書き方講座」

2024/09/04 - 2024/09/04
秋田県立秋田高校出前授業

秋田県立秋田高校出前授業

2024/05/29 - 2024/05/29
山形県立米沢興譲館高等学校出前授業

2022/10/03 - 2022/10/03
東北大学進学説明会

2022/07/03 - 2022/07/03
弘前高校出前授業

2020/10/26 - 2020/10/26
古川高校小講演会

2019/09/17 - 2019/09/17
東北大学サイエンスカフェ

2019/07/12 - 2019/07/12

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Media Coverage 5

血中濃度に性差のある元素・セレンと鉄代謝の関連性を発見－ICP-MSを用いた網羅的微量元素解析法を確立

日本経済新聞

2025/07

Type: Newspaper, magazine
不安定な必須微量元素セレンの安定な生体貯蔵法セレン欠乏に対する安定なセレン代謝利用の分子機構

2025/05

Type: Internet
東北大、食品成分スルフォラファンによる糖尿病増悪因子の制御を発見

2023/11

Type: Newspaper, magazine
東北大など、緑茶の成分に糖尿病の予防効果がある理由の一端を解明

マイナビニュース

2021/06

Type: Internet
糖尿病を悪化させるSePタンパク質の合成を抑制する新規RNAを発見

糖尿病リソースガイド

2021/06

Type: Internet

Academic Activities 7

Redox Week in Sendai 2025, Organizing Committee

2025/04/17 - 2025/04/21

Activity type: Academic society, research group, etc.
フォーラム2024 衛生薬学・環境トキシコロジーシンポジウム企画レドックス超分子・活性種研究の新潮流

2024/09/05 - 2024/09/05

Activity type: Academic society, research group, etc.
The XVIth International Congress of Toxicology（ICT2022）, planning of inter national symposium, Electrophiles-induced modification and biological response- Cutting edge research on oxidative stress for toxicology

2022/09/21 - 2022/09/21

Activity type: Academic society, research group, etc.
第2回レドックスR&D戦略委員会春のシンポジウム世話人

2022/03/04 - 2022/03/04

Activity type: Academic society, research group, etc.
STINT-JSPS Joint Symposium, Main Organizer

2022/10/28 - 2022

Activity type: Competition, symposium, etc.
生命金属科学第一回領域会議地方巡業（仙台）世話人

2021/01/23 - 2021/01/23

Activity type: Competition, symposium, etc.
第31回ビタミンE研究会世話人

2020/01/10 - 2020/01/11

Activity type: Academic society, research group, etc.

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