Review Article

Archives of Toxicology

, Volume 83, Issue 6, pp 519-548

Role of oxidative stress in alcohol-induced liver injury

  • Arthur I. CederbaumAffiliated withDepartment of Pharmacology and Systems Therapeutics, Mount Sinai School of Medicine Email author 
  • , Yongke LuAffiliated withDepartment of Pharmacology and Systems Therapeutics, Mount Sinai School of Medicine
  • , Defeng WuAffiliated withDepartment of Pharmacology and Systems Therapeutics, Mount Sinai School of Medicine

Rent the article at a discount

Rent now

* Final gross prices may vary according to local VAT.

Get Access

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.

Keywords

Oxidative stress Alcoholic liver injury Reactive oxygen species Antioxidants CYP2E1 TNFα