过氧化物还原蛋白
细胞凋亡
硫氧还蛋白
活性氧
程序性细胞死亡
化学
硫氧还蛋白还原酶
线粒体
分子生物学
细胞生长
癌细胞
过氧化氢
细胞生物学
癌症研究
生物
过氧化物酶
生物化学
氧化应激
癌症
酶
遗传学
作者
Larisa Nonn,Margareta Berggren,Garth Powis
出处
期刊:PubMed
日期:2003-07-01
卷期号:1 (9): 682-9
被引量:61
摘要
Peroxiredoxin-3 (Prdx3) is a mitochondrial member of the antioxidant family of thioredoxin peroxidases that uses mitochondrial thioredoxin-2 (Trx2) as a source of reducing equivalents to scavenge hydrogen peroxide (H(2)O(2)). Low levels of H(2)O(2) produced by the mitochondria regulate physiological processes, including cell proliferation, while high levels of H(2)O(2) are toxic to the cell and cause apoptosis. WEHI7.2 thymoma cells with stable overexpression of Prdx3 displayed decreased levels of cellular H(2)O(2) and decreased cell proliferation without a change in basal levels of apoptosis. Prdx3-transfected cells showed a marked resistance to hypoxia-induced H(2)O(2) formation and apoptosis. Prdx3 overexpression also protected the cells against apoptosis caused by H(2)O(2), t-butylhydroperoxide, and the anticancer drug imexon, but not by dexamethasone. Thus, mitochondrial Prdx3 is an important cellular antioxidant that regulates physiological levels of H(2)O(2), leading to decreased cell growth while protecting cells from the apoptosis-inducing effects of high levels of H(2)O(2).
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