苯乙基异硫氰酸酯和金诺芬诱导过氧化物酶 3 氧化与线粒体呼吸链的关系。
Mitochondrial respiratory chain involvement in peroxiredoxin 3 oxidation by phenethyl isothiocyanate and auranofin.
机构信息
National Research Centre for Growth and Development, Department of Pathology, University of Otago, Christchurch, New Zealand.
出版信息
FEBS Lett. 2010 Mar 19;584(6):1257-62. doi: 10.1016/j.febslet.2010.02.042. Epub 2010 Feb 19.
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.
线粒体过氧化物酶 3（Prx 3）在暴露于苯乙基异硫氰酸酯（PEITC）和金诺芬（AFN）的细胞中迅速氧化，但氧化机制尚不清楚。使用缺乏线粒体 DNA 的 HL-60 细胞，我们表明过氧化物酶 3 的氧化和细胞毒性需要一个功能正常的呼吸链。金诺芬可将硫氧还蛋白还原酶（TrxR）抑制高达 90%，而不会直接氧化过氧化物酶 3。然而，硫氧还蛋白还原酶的抑制作用与苯乙基异硫氰酸酯或安密妥合用可促进过氧化物酶 3 的氧化和细胞毒性。我们的结论是，过氧化物酶 3 的快速氧化是由于线粒体呼吸链产生的氧化剂增加所致。
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