Hepatoprotective effects of S-adenosyl-L-methionine against alcohol-and cytochrome P450 2E1-induced liver injury  

作　　者：Arthur I Cederbaum 

机构地区：[1]Department of Pharmacology and Systems Therapeutics, Box 1603, Mount Sinai School of Medicine, One Gustave Levy Place

出　　处：《World Journal of Gastroenterology》2010年第11期1366-1376,共11页世界胃肠病学杂志（英文版）

基　　金：Supported by NIH/NIAAA Grants No. AA017425;Supported by NIH/NIAAA Grants No. AA018790

摘　　要：S-adenosyl-L-methionine (SAM) acts as a methyl donor for methylation reactions and participates in the synthesis of glutathione. SAM is also a key metabolite that regulates hepatocyte growth, differentiation and death. Hepatic SAM levels are decreased in animal models of alcohol liver injury and in patients with alcohol liver disease or viral cirrhosis. This review describes the protection by SAM against alcohol and cytochrome P450 2E1-dependent cytotoxicity both in vitro and in vivo and evaluates mechanisms for this protection.S-adenosyl-L-methionine (SAM) acts as a methyl donor for methylation reactions and participates in the synthesis of glutathione. SAM is also a key metabolite that regulates hepatocyte growth, differentiation and death. Hepatic SAM levels are decreased in animal models of alcohol liver injury and in patients with alcohol liver disease or viral cirrhosis. This review describes the protection by SAM against alcohol and cytochrome P450 2E1-dependent cytotoxicity both in vitro and in vivo and evaluates mechanism...

关 键 词：Cytochrome P450 2E1 S-ADENOSYL-L-METHIONINE ETHANOL Toxic hepatitis Oxidative stress 

分 类 号：R575[医药卫生—消化系统]