Kato S, Alderman J, Lieber C S
Alcohol Research and Treatment Center, Bronx VA Medical Center, NY.
Alcohol Alcohol Suppl. 1987;1:231-4.
The participation of the microsomal ethanol oxidizing system (MEOS) and catalase in total ethanol metabolism is reviewed. Non-alcohol dehydrogenase (ADH) dependent pathways contribute to in vivo ethanol metabolism, but the respective role of each has long been debated. The principal data supporting a role for catalase is an occasionally reported moderate depression of ethanol metabolism after aminotriazole. In deermice lacking ADH, we observed a slight (though not statistically significant) decrease in basal ethanol metabolism of hepatocytes after aminotriazole. However, this decrease was found to parallel a similar inhibition of MEOS by aminotriazole, and thus may not reflect catalase mediated peroxidation in this animal. 1-butanol, a competitive inhibitor of ethanol oxidation by MEOS and not a substrate for catalase, decreased ethanol metabolism by hepatocytes in a concentration dependent manner. These results, as well as those from other investigators, indicate that MEOS mediates virtually all of non-ADH ethanol metabolism in vivo.
本文综述了微粒体乙醇氧化系统(MEOS)和过氧化氢酶在乙醇总代谢中的参与情况。非乙醇脱氢酶(ADH)依赖性途径对体内乙醇代谢有贡献,但每种途径的具体作用长期以来一直存在争议。支持过氧化氢酶起作用的主要数据是,氨基三唑给药后偶尔会报告乙醇代谢有中度抑制。在缺乏ADH的鹿鼠中,我们观察到氨基三唑给药后肝细胞基础乙醇代谢略有下降(尽管无统计学意义)。然而,发现这种下降与氨基三唑对MEOS的类似抑制作用平行,因此可能并不反映该动物中过氧化氢酶介导的过氧化作用。1-丁醇是MEOS氧化乙醇的竞争性抑制剂,不是过氧化氢酶的底物,它以浓度依赖的方式降低肝细胞的乙醇代谢。这些结果以及其他研究者的结果表明,MEOS实际上介导了体内所有非ADH依赖性乙醇代谢。