Role of oxidative stress in the pathogenesis of alcohol-induced liver disease

被引:107
作者
Sid, B. [1 ]
Verrax, J. [1 ]
Calderon, P. B. [1 ,2 ]
机构
[1] Catholic Univ Louvain, Louvain Drug Res Inst, Toxicol & Canc Biol Res Grp GTOX, B-1200 Brussels, Belgium
[2] Univ Arturo Prat, Fac Ciencias Salud, Iquique, Chile
关键词
alcohol; liver disease; oxidative damage; reactive oxygen species; MANGANESE SUPEROXIDE-DISMUTASE; CHRONIC ETHANOL-CONSUMPTION; HEPATIC STELLATE CELLS; TUMOR-NECROSIS-FACTOR; REACTIVE OXYGEN; VITAMIN-E; NADPH-OXIDASE; LIPID-PEROXIDATION; FATTY LIVER; MITOCHONDRIAL GLUTATHIONE;
D O I
10.3109/10715762.2013.819428
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Chronic alcohol consumption is a well-known risk factor for liver disease, which represents a major cause of morbidity and mortality worldwide. The pathological process of alcohol-induced liver disease is characterized by a broad spectrum of morphological changes ranging from steatosis with minimal injury to more advanced liver damage, including steato-hepatitis and fibrosis/cirrhosis. Experimental and clinical studies increasingly show that the oxidative damage induced by ethanol contribute in many ways to the pathogenesis of alcohol hepatotoxicity. This article describes the contribution of oxidative mechanisms to liver damage by alcohol.
引用
收藏
页码:894 / 904
页数:11
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