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Arch Toxicol. 2009 Jun;83(6):519-48. doi: 10.1007/s00204-009-0432-0. Epub 2009 May 16.

Role of oxidative stress in alcohol-induced liver injury.

Author information

1
Department of Pharmacology and Systems Therapeutics, Mount Sinai School of Medicine, Box 1603, One Gustave L Levy Place, New York, NY 10029, USA. Arthur.cederbaum@mssm.edu

Abstract

Reactive oxygen species (ROS) are highly reactive molecules that are naturally generated in small amounts during the body's metabolic reactions and can react with and damage complex cellular molecules such as lipids, proteins, or DNA. Acute and chronic ethanol treatments increase the production of ROS, lower cellular antioxidant levels, and enhance oxidative stress in many tissues, especially the liver. Ethanol-induced oxidative stress plays a major role in the mechanisms by which ethanol produces liver injury. Many pathways play a key role in how ethanol induces oxidative stress. This review summarizes some of the leading pathways and discusses the evidence for their contribution to alcohol-induced liver injury. Special emphasis is placed on CYP2E1, which is induced by alcohol and is reactive in metabolizing and activating many hepatotoxins, including ethanol, to reactive products, and in generating ROS.

PMID:
19448996
DOI:
10.1007/s00204-009-0432-0
[Indexed for MEDLINE]

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