Role of mitochondria in alcoholic liver injury

被引：121

作者：

Adachi, M ^{[1
]}

Ishii, H ^{[1
]}

机构：

[1] Keio Univ, Sch Med, Dept Internal Med, Shinjuku Ku, Tokyo 1608582, Japan

来源：

FREE RADICAL BIOLOGY AND MEDICINE | 2002年 / 32卷 / 06期

关键词：

oxidative stress; mitochondria; apoptosis; mitochondrial permeability transition; glutathione; cytochrome c; free radicals;

D O I：

10.1016/S0891-5849(02)00740-2

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：

Oxidative stress and oxygen-derived free radicals are well known to play an important role in the pathogenesis of ethanol-associated liver injury. Active oxidants produced during ethanol metabolism induce mitochondrial membrane depolarization and permeability changes in cultured hepatocytes. These mitochondrial alterations (loss of DeltaPsim and mitochondrial permeability transition [MPT]) are now recognized as a key step in apoptosis. In recent studies, including ours, the NIPT has been identified as a key step for the induction of mitochondrial cytochrome c release and caspase activation by ethanol. In addition, chronic and/or acute ethanol modulates intracellular, especially mitochondrial, antioxidant levels, leading to the increased susceptibility to alcoholic liver injury induced by several apoptotic stimuli. In this review, we address the mechanism of mitochondrial alterations and liver injury induced by ethanol. (C) 2002 Elsevier Science Inc.

引用

页码：487 / 491

页数：5

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