実験的肝障害に伴うラット肝薬物代謝酵素の変動

DOI NDLデジタルコレクション 日本農学文献記事索引 Web Site
  • 宮本 純之
    Research Department, Pesticides Division, Sumitomo Chemical Co., Ltd.
  • 奥野 泰由
    Research Department, Pesticides Division, Sumitomo Chemical Co., Ltd.
  • 門田 忠臣
    Research Department, Pesticides Division, Sumitomo Chemical Co., Ltd.
  • 三原 一優
    Research Department, Pesticides Division, Sumitomo Chemical Co., Ltd.

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  • Experimental Hepatic Lesions and Drug Metabolizing Enzymes in Rats

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Three types of experimental hepatic lesion were produced in male rats by subacute administration of carbon tetrachloride (CCl4), 4, 4′-diaminodiphenylmethane (DDM) and by feeding low protein-high fat diet (LPHF), characterized histopathologically by centrolobular fatty changes as well as fibrosis and cirrhosis, bile duct proliferation accompanied by cell infiltration and fibrosis, and diffuse fatty changes in parenchymal cells, respectively. Microsomal oxidation enzyme systems such as P-450, aniline hydroxylase, aminopyrine N-demethylase, p-nitrophenyl acetate hydrolase (carboxyesterase) and glutathione S-alkyltransferase were inhibited in the increasing order of DDM<CCl4≤LPHF, and the activity of the former 3 oxidation enzymes was generally more severely suppressed. Metabolism in vitro of 14C-fenitrothion and 14C-fenitrooxon by the hepatic enzyme preparations revealed that through 3 injured livers degradation of both compounds was affected to a lesser degree than activation of fenitrothion to fenitrooxon, majorly owing to less reduced activity of glutathione S-alkyltransferase.

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