Mitochondrial respiratory chain involvement in peroxiredoxin 3 oxidation by phenethyl isothiocyanate and auranofin
Mitochondrial respiratory chain involvement in peroxiredoxin 3 oxidation by phenethyl isothiocyanate and auranofin
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DOI：
10.1016/j.febslet.2010.02.042
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发表时间：
2010-03-19
期刊：
影响因子：
3.5
通讯作者：
Hampton, Mark B.
中科院分区：
文献类型：
--
作者：
Brown, Kristin K.;Cox, Andrew G.;Hampton, Mark B.
线粒体过氧化还原蛋白 3 (Prx 3) 在接触异硫氰酸苯乙酯 (PEITC) 和金诺芬 (AFN) 的细胞中迅速氧化，但氧化机制尚不清楚。使用消耗线粒体 DNA 的 HL-60 细胞，我们发现过氧化还原蛋白 3 氧化和细胞毒性需要功能性呼吸链。金诺芬可将硫氧还蛋白还原酶 (TrxR) 抑制高达 90%，而无需直接氧化过氧化还蛋白 3。然而，硫氧还蛋白还原酶的抑制与异硫氰酸苯乙酯或抗霉素 A 结合可促进过氧化还蛋白 3 氧化和细胞毒性。我们得出的结论是，过氧化还蛋白 3 快速氧化是由于线粒体呼吸链产生的氧化剂增加所致。 (C) 2010 年欧洲生化学会联合会。由 Elsevier B.V. 出版。保留所有权利。
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.