Oxidative Stress and Alcoholic Liver Disease

被引:281
作者
Wu, Defeng [1 ]
Cederbaum, Arthur I. [1 ]
机构
[1] Mt Sinai Sch Med, Dept Pharmacol & Syst Therapeut, New York, NY 10029 USA
关键词
Oxidative stress; alcoholic liver injury; reactive oxygen species; free radicals; antioxidants; TUMOR-NECROSIS-FACTOR; CHRONIC ETHANOL-CONSUMPTION; MITOCHONDRIAL PERMEABILITY TRANSITION; FREE-RADICAL MECHANISMS; MALONDIALDEHYDE-ACETALDEHYDE ADDUCTS; INCREASED LIPID-PEROXIDATION; RAT-LIVER; REACTIVE OXYGEN; CYTOCHROME-P450; 2E1; KUPFFER CELLS;
D O I
10.1055/s-0029-1214370
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
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. This review describes pathways involved in ROS formation, why ROS are toxic to cells, and how the liver protects itself against ROS. Acute and chronic ethanol treatment increases the production of ROS, lowers cellular antioxidant levels, and enhances oxidative stress in man), 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.
引用
收藏
页码:141 / 154
页数:14
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