Alcohol Potentiation of Liver Injury
Alcohol Potentiation of Liver Injury
复制标题
酒精增强肝损伤
DOI：
10.1016/0272-0590(84)90114-3
复制
发表时间：
1984
影响因子：
3.8
通讯作者：
O. Strubelt
中科院分区：
文献类型：
--
作者：
O. Strubelt
肝损伤的酒精增敏作用。胡晓明，陈晓华(1984).北京：科学出版社.APPL托昔康。4,144-151。酒精可以增强许多但不是所有肝毒性物质的活性。在这方面，不仅是高毒性剂量，而且是当今许多人通常消费的量。肝微粒体药物代谢系统的诱导导致肝毒性物质对有毒自由基的代谢增加是乙醇诱导的肝损伤加重的最已确定的原因。在CCl4的情况下，乙醇诱导的高代谢导致的肝脏缺氧可能参与了增强的肝毒性反应。肝毒素整体药代动力学的改变、肝脏谷胱甘肽的耗竭和脂质过氧化作用的增加似乎与乙醇对肝损伤的加重无关。经常饮酒的人被肝毒物质伤害的风险可能比戒酒的人高。因此，乙醇和其他肝毒性药物之间的相互作用应被视为乙醇引起的人类肝损伤的一个可能的额外因素，至少部分解释了人类对酒精肝毒性影响的敏感性的巨大差异。
Alcohol Potentiation of Liver Injury. STRUBELT, O. (1984).Fundam. Appl. Toxicol. 4, 144–151. Alcohol enhances the activity of many but not of all hepatotoxic agents. Not only high toxic doses but also amounts commonly consumed today by many people are active in this respect. An induction of the hepatic microsomal drug-metabolizing system leading to an increased metabolism of the hepatotoxic agents to toxic radicals is the best established cause for ethanol-induced potentiation of liver injury. In the case of CCl4, hepatic hypoxia resulting from an ethanol-induced hypermetabolism may participate in the enhanced hepatotoxic response. Changes in the overall pharmacokinetics of the hepatotoxins, depletion of hepatic glutathione, and an increase of lipid peroxidation seem not to be implicated in potentiation of liver injury by ethanol. People regularly consuming alcohol may run a higher risk of being injured by hepatotoxic agents than abstainers. Thus, interactions between ethanol and other hepatotoxic agents should be envisaged as a possible additional factor in ethanol-induced human liver damage explaining, at least partially, the great variation in the sensitivity of man to the hepatotoxic effects of alcohol.
乙醇增强可卡因引起的肝毒性。
影响因子：
5.8
作者：
Smith,AC;Freeman,RW;Harbison,RD
通讯作者：
Harbison,RD
维生素 A 和乙醇对大鼠的肝毒性。
影响因子：
29.4
作者：
Leo,MA;Arai,M;Sato,M;Lieber,CS
通讯作者：
Lieber,CS