Hepatic function after acute of subchronic nicotine administration in untreated mice and mice treated with hepatotoxic chemicals.
Male mice treated with nicotine hydrochloride either acutely (5 mg/kg i.p.) or subchronically (5 mg/kg i.p. daily for 3 weeks; 25 mg/liter in drinking water for 2-3 months) showed no evidence of hepatic dysfunction, as measured by serum glutamic-pyruvic transaminase or serum alkaline phosphatase activities. Neither acute nor subchronic administration modified the hepatotoxic response to a potent hepatotoxin (carbon tetrachloride), nor that of less potent hepatotoxins chloroform or 1, 1, 1-trichloroethane, nor was the cholestatic effect of alpha-naphthylisothiocyanate modified.
D015058:1-Naphthylisothiocyanate / Q000494:pharmacology; D000410:Alanine Transaminase / Q000097:blood; D000469:Alkaline Phosphatase / Q000097:blood; D000818:Animals; D001663:Bilirubin / Q000097:blood; D056486:Chemical and Drug Induced Liver Injury / Q000503:physiopathology*; D006843:Hydrocarbons, Chlorinated / Q000494:pharmacology; D007928:Lethal Dose 50; D008099:Liver / Q000187:drug effects*; D008297:Male; D051379:Mice; D009538:Nicotine / Q000494:pharmacology* / Q000633:toxicity
D006843:Hydrocarbons, Chlorinated; D015058:1-Naphthylisothiocyanate; D009538:Nicotine; D000410:Alanine Transaminase; D000469:Alkaline Phosphatase; D001663:Bilirubin