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HERO ID
2919665
Reference Type
Journal Article
Subtype
Review
Title
Alcohol and mitochondria: A dysfunctional relationship
Author(s)
Hoek, JB; Cahill, A; Pastorino, JG
Year
2002
Is Peer Reviewed?
Yes
Journal
Gastroenterology
ISSN:
0016-5085
EISSN:
1528-0012
Volume
122
Issue
7
Page Numbers
2049-2063
Language
English
PMID
12055609
DOI
10.1053/gast.2002.33613
Web of Science Id
WOS:000176280300036
URL
http://www.gastrojournal.org/article/S0016-5085(02)00037-9/abstract
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Abstract
Mitochondria are intimately involved in the generation of and defense against reactive oxygen species (ROS). Mitochondria are themselves targets of oxidative stress and also contribute to mechanisms by which oxidative stress-related signals control cell fate. Ethanol promotes oxidative stress, both by increasing ROS formation and by decreasing cellular defense mechanisms. These effects of ethanol are prominent in the liver, the major site of ethanol metabolism in the body. The question remains to what extent this contributes to ethanol-dependent tissue damage or the susceptibility of cells to other stressors. In this review, we consider how mitochondrial actions of ethanol influence oxidative stress management of liver cells. Mitochondrial electron transport constitutes the major intracellular source of ROS, and ethanol treatment imposes conditions that promote ROS formation by mitochondria, the effects of which may be enhanced by a decrease in mitochondrial oxidative stress defenses. A significant target of ethanol-related increases in oxidative stress is mitochondrial DNA. Ethanol-induced damage to mitochondrial DNA, if not adequately repaired, impairs mitochondrial function, which further increases oxidative stress in the cell, leading to a vicious cycle of accumulating cell damage that is more apparent with advancing age. Uncontrolled mitochondrial formation of ROS promotes the inappropriate activation of the mitochondrial permeability transition, increasing the sensitivity of cells to other pro-apoptotic or damage signals. In combination with ethanol-induced defects in mitochondrial function, these alterations may promote both apoptotic and necrotic cell death in response to otherwise benign or beneficial challenges and contribute to the onset or progression of alcohol-induced liver diseases.
Tags
IRIS
•
n-Butanol
• Cited 2016 Public Comment Draft
Tox Review
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