Carbon tetrachloride-induced early biochemical alterations but not necrosis in pigeon's liver.
In contrast to what is well known to occur in rats, pigeons receiving CCl4 (1 ml/kg i.p.) were not susceptible to necrogenic effects of the hepatotoxin at 24 h. There were, however, other early biochemical alterations observable, such as depression of glucose 6 phosphatase activity, decrease in the cytochrome P-450 content and in aminopyrine-N-demethylase activity in pigeon liver microsomes at 3 and 6 h after CCl4 administration. Pigeon liver was able to activate CCl4 to reactive metabolites that bind covalently to lipids, but no CCl4-induced lipid peroxidation was proved by the diene hyperconjugation technique in pigeon liver microsomes at 1, 3 or 6 h after administration. Results suggest that covalent binding of CCl4-reactive metabolites are more relevant to early biochemical alterations induced by CCl4 than is lipid peroxidation. Absence of CCl4-induced necrosis in pigeon liver could be attributable to a smaller intensity of covalent binding interactions observed, when compared to susceptible species, and to absence of lipid peroxidation.
D000633:Aminopyrine N-Demethylase / Q000378:metabolism; D000818:Animals; D002252:Carbon Tetrachloride Poisoning / Q000378:metabolism* / Q000473:pathology; D010856:Columbidae; D003577:Cytochrome P-450 Enzyme System / Q000378:metabolism; D005952:Glucose-6-Phosphatase / Q000378:metabolism; D066298:In Vitro Techniques; D007521:Isocitrate Dehydrogenase / Q000378:metabolism; D008054:Lipid Peroxides / Q000378:metabolism; D008099:Liver / Q000187:drug effects / Q000378:metabolism* / Q000473:pathology; D008862:Microsomes, Liver / Q000201:enzymology; D009336:Necrosis; D051381:Rats; D013045:Species Specificity
D008054:Lipid Peroxides; D003577:Cytochrome P-450 Enzyme System; D007521:Isocitrate Dehydrogenase; D000633:Aminopyrine N-Demethylase; D005952:Glucose-6-Phosphatase