Possible Mechanism of Liver Necrosis Caused by Aromatic Organic Compounds
- 1 January 1971
- journal article
- Published by Proceedings of the National Academy of Sciences in Proceedings of the National Academy of Sciences of the United States of America
- Vol. 68 (1), 160-164
- https://doi.org/10.1073/pnas.68.1.160
Abstract
Treatment of rats with phenobarbital, which stimulates the activity of the drug-metabolizing enzymes in the liver, potentiates hepatic necrosis elicited by bromobenzene and a number of other chemically inert halogenated aromatic hydrocarbons. Radioautographic studies indicate that [(14)C]bromobenzene is covalently bound at the sites of necrosis. From these results, it is inferred that the hepatotoxic effects of the halogenated aromatic hydrocarbons are mediated by chemically active metabolites formed in hepatocytes. In accord with this view, a number of aromatic halogenated hydrocarbons are converted by microsomes in vitro to active intermediates which form covalent complexes with glutathione (GSH).This publication has 7 references indexed in Scilit:
- 1,2-Naphthalene oxide as an intermediate in the microsomal hydroxylation of naphthalene. VBiochemistry, 1970
- The role of arene oxide-oxepin systems in the metabolism of aromatic substrates. III. Formation of 1,2-naphthalene oxide from naphthalene by liver microsomesJournal of the American Chemical Society, 1968
- Phenobarbital-induced fine structural changes in rat liver.1966
- An enzyme from rat liver catalysing conjugations with glutathioneBiochemical Journal, 1961
- Metabolism of polycyclic compounds. 17. The reaction of 1:2-dihydronaphthalene and 1:2-epoxy-1:2:3:4-tetrahydronaphthalene with glutathione catalysed by tissue preparationsBiochemical Journal, 1960
- [Effect of penicillin on liver necroses].1954
- Mechanism of the potentiating action of beta-diethylaminoethyl diphenylpropylacetate.1954