The glutathione-linked metabolism of 2-allyl-2-isopropy-lacetamide in rats. Further evidence for the formation of a reactive metabolite
Author:
Publisher
Elsevier BV
Subject
Toxicology,General Medicine
Reference19 articles.
1. Rapid loss of cytochrome P-450 and haem caused in the liver microsomes by the porphyrogenic agent 2-allyl-2-isopropylacetamide;De Matteis;FEBS Lett.,1970
2. Chemically induced porphyria. Increased microsomal heme turnover after treatment with allyl-isopropylacetamide;Meyer;Science,1971
3. Decreased levels of cytochrome P-450 and catalase in hepatic porphyria caused by substituted acetamides and barbiturates;Abbritti;Chem.-Biol. Interact.,1971
4. Loss of haem in rat liver caused by the porphyrogenic agent 2-allyl-2-isopropylacetamide;De Matteis;Biochem. J.,1971
5. Incorporation of radioactive δ-aminolevulinic acid into microsomal cytochrome P-450. Selective breakdown of the hemoprotein by allylisopropyl acetamide and carbon tetrachloride;Levin;Arch. Biochem. Biophys.,1972
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1. Allylisopropylacetamide induces rat hepatic ornithine decarboxylase;Journal of Biochemical Toxicology;1987
2. Evidence for thein vitro metabolism of allylisopropylacetamide to reactive intermediates. Mechanistic studies with oxygen-18;Biological Mass Spectrometry;1984-07
3. New Developments in the Regulation of Heme Metabolism and Their Implications;CRC Critical Reviews in Toxicology;1984-01
4. Iron loading of cultured hepatocytes. Effect of iron on 5-aminolaevulinate synthase is independent of lipid peroxidation;Biochemical Journal;1983-05-15
5. The destruction of cytochrome P-450 by alclofenac: Possible involvement of an epoxide metabolite;Biochemical Pharmacology;1982-01
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