Bailey Shannon M, Cunningham Carol C
Department of Environmental Health Sciences, School of Public Health, University of Alabama at Birmingham, 1530 3rd Ave. South, RPHB 317, Birmingham, AL 35294, USA.
Free Radic Biol Med. 2002 Jan 1;32(1):11-6. doi: 10.1016/s0891-5849(01)00769-9.
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.
氧化应激在酒精性肝病发展中的重要性早已得到认可。然而，乙醇引发肝脏中活性氧增加的机制很复杂，最近的研究结果表明，线粒体可能在急性或慢性接触乙醇的肝细胞中氧化剂水平的总体增加中起重要作用。本综述聚焦于一些观察结果，这些结果表明乙醇增加线粒体活性氧产生的能力与其通过氧化过程的代谢和/或乙醇相关的线粒体电子传递链改变有关。此外，乙醇引发的活性氧增加对线粒体蛋白质进行氧化修饰并使其失活的能力被强调为乙醇可能进一步破坏线粒体结构和功能的一种机制。
