Reversible oxidation of mitochondrial peroxiredoxin 3 in mouse heart subjected to ischemia and reperfusion

被引：41

作者：

Kumar, Vikas ^{[1
]}

Kitaeff, Nailya ^{[2
]}

Hampton, Mark B. ^{[1
]}

Cannell, Mark B. ^{[2
]}

Winterbourn, Christine C. ^{[1
]}

机构：

[1] Univ Otago Christchurch, Dept Pathol, Christchurch, New Zealand

[2] Univ Auckland, Dept Physiol, Auckland, New Zealand

来源：

FEBS LETTERS | 2009年 / 583卷 / 06期

关键词：

Cardiac ischemia; Reperfusion injury; Mitochondria; Peroxiredoxin; Hydrogen peroxide; OXIDANT STRESS; INJURY; MYOCARDIUM; MECHANISMS; PROTEOME;

D O I：

10.1016/j.febslet.2009.02.018

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：

Peroxiredoxins decompose peroxides through reversible oxidation of their active site cysteines. The redox state of the 2-Cys peroxiredoxins, 1, 2 and 3, was investigated in mouse hearts undergoing ischemia and reperfusion in a Langendorff system. The peroxiredoxins were predominantly reduced in control hearts. Mitochondrial peroxiredoxin 3 underwent significant oxidation to its disulfide-linked dimer during ischemia. Oxidation was largely reversed during reperfusion. No redox changes in cytoplasmic peroxiredoxins 1 and 2 were apparent. Peroxiredoxin 3 oxidation suggests localized mitochondrial generation of reactive oxidants during ischemia. This local antioxidant activity of peroxiredoxin 3 may have a role in maintaining cardiac function. (C) 2009 Federation of European Biochemical Societies. Published by Elsevier B. V. All rights reserved.

引用

页码：997 / 1000

页数：4

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