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TCDD-induced changes in rat liver microsomal enzymes.
Author(s) -
George W. Lucier,
Otelia S. McDaniel,
Gary E. R. Hook,
Bruce A. Fowler,
Babasaheb Sonawane,
Edward J. Faeder
Publication year - 1973
Publication title -
environmental health perspectives
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.257
H-Index - 282
eISSN - 1552-9924
pISSN - 0091-6765
DOI - 10.1289/ehp.7305199
Subject(s) - chemistry
2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD), a contaminant of the herbicide 2,4,5trichlorophenoxyacetic acid (2,4,5-T), is extremely toxic (1), although the mechanism of toxicity is not known. Other papers presented at this conference cover the spectrum of environmental and health hazards of chlorinated dibenzodioxins and dibenzofurans. It should suffice to say here that these compounds are teratogens (2-4) in rodents, and the extensive use of 2,4,5-T, especially in Vietnam, has focused concern on their potential health hazards. Recently TCDD was shown to be an inducer of 8-aminolevulinic acid synthetase in the chick embryo (5) and also to decrease hexobarbital sleeping times in rats (6). These reports prompted us to investigate the effects of sublethal doses of TCDD on activities of hepatic microsomal and mitochondrial enzymes. The microsomal enzymes include components that are involved in the detoxication of foreign compounds and the regulation of many endogenous compounds such as the steroid hormones (7). Microsomal constituents and activities investigated in this study were: cytochrome P-450, cytochrome b5,

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