Dose-dependent modification of 1,1-dichloroethylene toxicity by acetone.
The ability of acetone to potentiate the toxicity of 1,1-dichloroethylene (DCE) in male rats was investigated. A biphasic potentiation of DCE-induced hepatotoxicity was observed; low doses (5 and 10 mmol/kg, p.o.) of acetone were active, whereas higher doses (15 and 30 mmol/kg) were not. Nephrotoxicity was not affected.
D000096:Acetone / Q000633:toxicity*; D000410:Alanine Transaminase / Q000097:blood; D000818:Animals; D001806:Blood Urea Nitrogen; D056486:Chemical and Drug Induced Liver Injury; D004000:Dichloroethylenes / Q000633:toxicity*; D004357:Drug Synergism; D006843:Hydrocarbons, Chlorinated / Q000633:toxicity*; D007674:Kidney Diseases / Q000139:chemically induced*; D008297:Male; D009929:Organ Size / Q000187:drug effects; D009954:Ornithine Carbamoyltransferase / Q000097:blood; D051381:Rats; D011919:Rats, Inbred Strains; D013757:Tetraethylammonium Compounds / Q000378:metabolism; D010130:p-Aminohippuric Acid / Q000378:metabolism
D004000:Dichloroethylenes; D006843:Hydrocarbons, Chlorinated; D013757:Tetraethylammonium Compounds; D000096:Acetone; C029297:vinylidene chloride; D009954:Ornithine Carbamoyltransferase; D000410:Alanine Transaminase; D010130:p-Aminohippuric Acid