期刊
FEBS LETTERS
卷 584, 期 6, 页码 1257-1262出版社
WILEY
DOI: 10.1016/j.febslet.2010.02.042
关键词
Hydrogen peroxide; Redox signaling; Oxidative stress; Thioredoxin reductase; Thioredoxin; Mitochondria
资金
- Cancer Society of New Zealand
- Health Research Council of New Zealand
- Tertiary Education Commission of New Zealand
Mitochondrial peroxiredoxin 3 (Prx 3) is rapidly oxidized in cells exposed to phenethyl isothiocyanate (PEITC) and auranofin (AFN), but the mechanism of oxidation is unclear. Using HL-60 cells deplete of mitochondrial DNA we show that peroxiredoxin 3 oxidation and cytotoxicity requires a functional respiratory chain. Thioredoxin reductase (TrxR) could be inhibited by up to 90% by auranofin without direct oxidation of peroxiredoxin 3. However, inhibition of thioredoxin reductase promoted peroxiredoxin 3 oxidation and cytotoxicity in combination with phenethyl isothiocyanate or antimycin A. We conclude that rapid peroxiredoxin 3 oxidation occurs as a consequence of increased oxidant production from the mitochondrial respiratory chain. (C) 2010 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据