Hassing J M, Hupka A L, Stohs S J, Yoon P C
Res Commun Chem Pathol Pharmacol. 1979 Aug;25(2):389-94.
Ethanol oxidation is accomplished primarily by alcohol dehydrogenase. However, a microsomal system involving hydrogen peroxide formation operates at elevated ethanol concentrations. Removal of the resultant hydrogen peroxide may depend on the activity of glutathione peroxidase. In the study, we have examined the effect of chronic ethanol exposure on hepatic glutatione levels and found that ethanol exposure resulted in elevations of hepatic reduced and oxidized glutathione. The dietary inclusion of the sulfhydryl amino acid, D-penicillamine, increased hepatic reduced glutathione (GSH) in both ethanol-dependent and control rats. However, D-penicillamine did not have a differential effect on hepatic GSH when comparing ethanol-dependent and control animals. Following two weeks exposure, the exclusion of ethanol and/or D-penicillamine from the diet for 24 hours resulted in a significant decrease in hepatic GSH.
乙醇氧化主要由乙醇脱氢酶完成。然而，一个涉及过氧化氢形成的微粒体系统在乙醇浓度升高时起作用。所产生的过氧化氢的清除可能取决于谷胱甘肽过氧化物酶的活性。在该研究中，我们检测了长期乙醇暴露对肝脏谷胱甘肽水平的影响，发现乙醇暴露导致肝脏还原型和氧化型谷胱甘肽水平升高。在饮食中添加巯基氨基酸D-青霉胺，可使乙醇依赖型和对照大鼠的肝脏还原型谷胱甘肽（GSH）增加。然而，比较乙醇依赖型和对照动物时，D-青霉胺对肝脏GSH没有差异影响。暴露两周后，从饮食中排除乙醇和/或D-青霉胺24小时，导致肝脏GSH显著下降。
