Oxidative damage to the hepatocellular proteins after chronic ethanol intake in the rat

Abstract

Background: Protein carbonyl content, a measure of oxidative damage to hepatocellular proteins, and the activities of some thiol-containing proteins were assayed in the liver and plasma, as thiol-containing protein, appear to be targets for free radicals. These may be important in the mechanism of ethanol-induced liver injury.

Methods: Tap water containing ethanol at the concentration of 25% (v/v) and phenobarbital (500 mg/l) was the only source of drinking water for the experimental rats for 24 months. Another group of rats were administered 25% (v/v) ethanol alone in drinking water for 24 months. Control rats were administered either phenobarbital alone in drinking water or tap water for 24 months. At the end of 24 months, the rats were sacrificed. The protein carbonyl content, activities of glutamine synthase and biotinidase-sulfhydryl group containing enzymes were assayed in the liver along with alkaline protease, an enzyme that degrades oxidized proteins. The total thiol, albumin and the activity of biotinidase were measured in the plasma.

Results: The protein carbonyl content of the liver was increased in the ethanol/phenobarbital-treated rats as well as in the ethanol-treated rats as compared with the controls. The activities of glutamine synthase and biotinidase were decreased significantly in the livers of ethanol/phenobarbital-treated rats as well as the ethanol-treated rats as compared with the controls. The activity of alkaline protease was increased significantly in both the ethanol-treated groups. In the plasma of ethanol/phenobarbital-treated rats as well as the ethanol-treated rats total thiol, albumin and the activity of biotinidase were decreased significantly as compared with the controls. The ethanol/phenobarbital-treated rats as well as the ethanol-treated rats developed fatty liver.

Conclusions: Damage to proteins occurs upon chronic ethanol intake in the rat, and it may play a role in the pathogenesis of alcohol-induced fatty liver.