Contribution of mitochondria to oxidative stress associated with alcoholic liver disease

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.

Publication types

  • Review

MeSH terms

  • Alcohol Drinking / metabolism
  • Animals
  • Ethanol / metabolism
  • Ethanol / pharmacology
  • Hepatocytes / metabolism
  • Humans
  • Liver Diseases, Alcoholic / metabolism*
  • Mitochondria / metabolism*
  • Mitochondrial Proteins / metabolism*
  • Oxidation-Reduction
  • Oxidative Phosphorylation / drug effects
  • Oxidative Stress / physiology*
  • Rats
  • Reactive Oxygen Species / metabolism*


  • Mitochondrial Proteins
  • Reactive Oxygen Species
  • Ethanol