Résumé
During the last decades a vast number of reports have aimed at elucidating the mechanisms behind alcohol-related organ injury, but the manner in which ethanol induces, e.g., liver damage is still an enigma. Increased oxidative stress has been put forward has been put forward as one possible mechanism behind alcohol-related tissue damage. This paper focuses on the effect of chronic ethanol consumption on antioxidant status and lipid peroxide levels in blood and liver of rats. Alcohol was given twice daily in a total dose of 5 g ethanol/kg body wt. per day divided into two 2.5 g ethanol/kg body wt. doses as a 50% water solution, by gavage over 4 weeks. Chronic ethanol ingestion led neither to a significant change in lipid peroxide formation nor to a significant change in enzymatic antioxidant activities. Only concentrations of oxidized glutathione and of other non-enzymatic antioxidants such as vitamin E showed a tendency to decrease after alcohol application. The data presented could serve to emphasize no involvement of free radical-induced lipoperoxidation in the pathogenesis of ethanolic liver diseases.