Mitochondrial respiratory chain involvement in peroxiredoxin 3 oxidation by phenethyl isothiocyanate and auranofin

被引：29

作者：

Brown, Kristin K.

Cox, Andrew G.

Hampton, Mark B. ^{[1
]}

机构：

[1] Univ Otago, Free Rad Res Grp, Christchurch, New Zealand

来源：

FEBS LETTERS | 2010年 / 584卷 / 06期

关键词：

Hydrogen peroxide; Redox signaling; Oxidative stress; Thioredoxin reductase; Thioredoxin; Mitochondria; BETA-PHENYLETHYL ISOTHIOCYANATE; REDOX-MEDIATED MECHANISM; THIOREDOXIN REDUCTASE; CANCER-CELLS; HYDROGEN-PEROXIDE; DIETARY ISOTHIOCYANATES; DEPENDENT APOPTOSIS; TRIGGERS APOPTOSIS; GOLD(I) COMPOUNDS; SENSITIZES CELLS;

D O I：

10.1016/j.febslet.2010.02.042

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

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.

引用

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页码：1257 / 1262

页数：6

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