Increased carbon tetrachloride hepatotoxicity after low-level ethanol consumption.
Male rats provided with a 5 or 15% (v/v) ethanol solution as the sole source of fluid consumed ethanol at a rate of 11.4 or 24.9% of total calories (4.2 or 8.3 g/kg daily). After ethanol consumption lasting 1, 2 and 3 weeks the hepatotoxicity of CCl4 (0.1 ml/kg i.p.) was elevated by determination of serum activities of glutamic-oxaloacetic transaminase (GOT), glutamic-pyruvic transaminase ( GPT), sorbitol dehydrogenase (SDH) and histological investigations. Carbon tetrachloride (CCl4)-induced liver damage was significantly greater in rats provided with ethanol than in the tap-water consuming controls. This potentiation of CCl4 hepatotoxicicty was fully developed already after a 1-week exposition to ethanol and was greater in the 15% than in the 5% ethanol group. Ethanol alone did not influence serum enzyme activities but increased microsomal aniline hydroxylation. There was, however, no clear-cut parallelism between potentiation of CCl4 hepatotoxicity and activation of aniline hydroxylation.
D000815:Aniline Hydroxylase / Q000378:metabolism; D000818:Animals; D001835:Body Weight; D002252:Carbon Tetrachloride Poisoning / Q000378:metabolism / Q000503:physiopathology*; D056486:Chemical and Drug Induced Liver Injury / Q000209:etiology*; D004357:Drug Synergism; D004798:Enzymes / Q000097:blood; D000431:Ethanol / Q000097:blood / Q000633:toxicity*; D005247:Feeding Behavior; D008297:Male; D051381:Rats
D004798:Enzymes; D000431:Ethanol; D000815:Aniline Hydroxylase