シスチン要求性アンチポーターを介した過剰な活性イオウ分子の細胞外排出

青木 はな子; 秋山 雅博; 鵜木 隆光; 蕨 英治; 西村 明幸; 西田 基宏; 熊谷 嘉人

doi:10.14869/toxpt.49.1.0_O-38

The 49th Annual Meeting of the Japanese Society of Toxicology

Session ID : O-38

DOI https://doi.org/10.14869/toxpt.49.1.0_O-38

Conference information

Host: The Japanese Society of Toxicology

Name : The 49th Annual Meeting of the Japanese Society of Toxicology

Date : June 30, 2022 - July 02, 2022

Oral Session

Export of excess reactive sulfur species through cystine-dependent antiporters

*Hanako AOKI, Masahiro AKIYAMA, Takamitsu UNOKI, Eiji WARABI, Akiyuki NISHIMURA, Motohiro NISHIDA, Yoshito KUMAGAI

Author information

*Hanako AOKI
Degree Programs in Medical Sciences, Graduate School of Comprehensive Human Sciences, University of Tsukuba
Masahiro AKIYAMA
Faculty of Medicine, University of Tsukuba
Faculty of Pharmacy, Keio University
Takamitsu UNOKI
Faculty of Medicine, University of Tsukuba
Hygienic Chemistry Section, Department of Basic Medical Sciences, National Institute for Minamata Disease
Eiji WARABI
Degree Programs in Medical Sciences, Graduate School of Comprehensive Human Sciences, University of Tsukuba
Faculty of Medicine, University of Tsukuba
Akiyuki NISHIMURA
Division of Cardiocirculatory Signaling, National Institute for Physiological Sciences
Motohiro NISHIDA
Division of Cardiocirculatory Signaling, National Institute for Physiological Sciences
Yoshito KUMAGAI
Degree Programs in Medical Sciences, Graduate School of Comprehensive Human Sciences, University of Tsukuba
Faculty of Medicine, University of Tsukuba

CONFERENCE PROCEEDINGS FREE ACCESS

Details

Abstract

Reactive sulfur species (RSS) exhibit high nucleophilicity/antioxidative property and thus is thought to play an important role in repressing electrophilic/oxidative stress. On the other hand, excess amount of RSS (sulfur stress) may disrupt redox homeostasis and increase health risk. Here, we examined adaptive response against intracellular sulfur stress. The present study suggests that there are cystine-dependent antiporters including SLC7A11 to excrete excess intracellular CysSSH.

Corresponding author

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