No response of pigeon liver to dimethylnitrosamine acute effects.
No evidence for liver necrosis was observed at 24, 48 or 72 h after injection of dimethylnitrosamine (DMN) (70 mg/kg, i.p.) to pigeons. The assessment of possible liver necrosis was made by determination of isocitric dehydrogenase (ICD), glutamate oxalacetate transaminase (GOT) and glutamate pyruvate transaminase (GPT) in plasma. The ability of pigeon liver slices to metabolize CO2 or to give covalent binding of reactive metabolites to nucleic acids was 24 times smaller than that for rat. Similarly, the pigeon liver microsomes or 9000 X g supernatant have DMN-demethylase activity or ability to activate DMN to reactive metabolites that bind covalently to proteins very close to zero. Results suggest that resistance of pigeon liver to DMN acute effects is related to its lack of ability for DMN metabolic activation.
D000410:Alanine Transaminase / Q000097:blood; D000818:Animals; D001219:Aspartate Aminotransferases / Q000097:blood; D002245:Carbon Dioxide / Q000378:metabolism; D010856:Columbidae; D019392:Cytochrome P-450 CYP2E1; D004128:Dimethylnitrosamine / Q000494:pharmacology*; D007521:Isocitrate Dehydrogenase / Q000097:blood; D008099:Liver / Q000187:drug effects* / Q000378:metabolism; D008297:Male; D008862:Microsomes, Liver / Q000378:metabolism; D010089:Oxidoreductases, N-Demethylating / Q000097:blood; D051381:Rats
D002245:Carbon Dioxide; D007521:Isocitrate Dehydrogenase; D019392:Cytochrome P-450 CYP2E1; D010089:Oxidoreductases, N-Demethylating; D001219:Aspartate Aminotransferases; D000410:Alanine Transaminase; D004128:Dimethylnitrosamine