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• W1528674127 abstract "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." @default.
• W1528674127 created "2016-06-24" @default.
• W1528674127 creator A5047734216 @default.
• W1528674127 creator A5077827778 @default.
• W1528674127 date "2002-01-01" @default.
• W1528674127 modified "2023-10-02" @default.
• W1528674127 title "Contribution of mitochondria to oxidative stress associated with alcoholic liver disease1 1This article is part of a series of reviews on “Alcohol, Oxidative Stress and Cell Injury”. The full list of papers may be found on the homepage of the journal." @default.
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• W1528674127 doi "https://doi.org/10.1016/s0891-5849(01)00769-9" @default.
• W1528674127 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/11755312" @default.
• W1528674127 hasPublicationYear "2002" @default.
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