An In Vitro Model for Studying Cellular and Molecular Mechanisms of Thymic Atrophy Induced by Chlorinated Aromatic Compounds

作者: William F. Greenlee , Karen M. Dold , Rosemarie Osborn

DOI: 10.1007/978-94-009-4307-0_13

关键词:

摘要: 2, 3, 7, 8-Tetrachlorodibenzo-p-dioxin (TCDD) is the prototype for certain isomers from several classes of halogenated aromatic compounds, including polychlorinated biphenyls (Goldstein, 1980; Poland et al., 1979). Studies carried out in inbred murine strains have shown that induction cytochrome P1-450 and other xenobiotic metalbolizing enzymes by TCDD regulated a genetic locus (designated Ah locus) (reviewed Knutson, 1982; Nebert Jensen, It has been postulated (Nebert 1984; 1979), codes receptor Protein (to be designated this report as receptor). The originally was identified liver (Poland 1976) subsequently detected epithelial tissues (Glasiewicz, 1983) animal (Guenthner Nebert, 1977) human (Hudson cells culture. In mice to involved two toxic responses TCDD: epidermal hyperplasia (Knutson Poland, 1982) thymic atrophy Glover, see below). actions on targets such skin thymus appear result altered patterns growth differentiation Greenlee Neal, 1985).

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