Contribution of mitochondria to oxidative stress associated with alcoholic liver disease

被引:237
作者
Bailey, SM
Cunningham, CC
机构
[1] Univ Alabama, Sch Publ Hlth, Dept Environm Hlth Sci, Birmingham, AL 35294 USA
[2] Wake Forest Univ, Sch Med, Dept Biochem, Winston Salem, NC 27109 USA
关键词
alcohol; mitochondria; oxidative stress; reactive oxygen species; NADH ubiquinone reductase; ubiquinone-cytochrome c reductase; semiquinone anion; free radical;
D O I
10.1016/S0891-5849(01)00769-9
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 [生物化学与分子生物学]; 081704 [应用化学];
摘要
The importance of oxidative stress in the development of alcoholic liver disease has long been appreciated. The mechanism by which ethanol triggers an increase in reactive oxygen species in the liver is complex, however, recent findings suggest that the mitochondrion may contribute significantly to the overall increase in oxidant levels in hepatocytes exposed to ethanol acutely or chronically. This review is focused on observations which indicate that the ability of ethanol to increase mitochondrial reactive oxygen species production is linked to its metabolism via oxidative processes and/or ethanol-related alterations to the mitochondrial electron transport chain. Furthermore. the capacity of ethanol-elicited increases in reactive oxygen species to oxidatively modify and inactivate mitochondrial proteins is highlighted as a mechanism by which ethanol might further disrupt the structure and function of mitochondria. (C) 2001 Elsevier Science Inc.
引用
收藏
页码:11 / 16
页数:6
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