Developmental Landmarks in Offspring of Rats Exposed Singly, and in Combination to Aroclor 1016 and Levo-Thyroxine
Bulletin of Environmental Contamination Toxicology
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Polychlorinated biphenyls (PCBs) have been associated with a reduction in circulating thyroid hormones (TH) (Desaulniers et al. 1997) and arc speculated to interact with this system to alter normal development (reviewed in Brouwer et al. 1998: Porterfield and Hendry 1998). To date, most concern over PCB exposure has been with higher chlorinated and coplanar mixtures which have poor or minimal interaction with the thyroid hormone system when compared to the more infrequently studied mono-, di- and tri-ortho substituted CBs, which arc more readily metabolized to hydroxylated metabolites (Hansen 1998). Nonplanar PCBs and hydroxylated PCB metabolites however, arc prevalent as transient and pulsatile components in fish human serum, (Gerstenberger and Hansen, 2000) and breast milk, (Kostyniak et al. 1999) and arc major products of environmental and laboratory dechlorination reactions (Brown et al. 1987). HydroxyIated PCB metabolites can inhibit thyroid hormone sulfation, (reviewed in Brouwer et al. 1998) and Kato et al.(1998) related reductions in serum T4 in rats to methylsulfonyl metabolites of PCBs. T4 concentrations were severely reduced in animals exposed 10 a tetraCB, (Brouwer and Van Den Berg 1986) and based on the similarity between TH nuclear receptors and PCB congeners with three chlorine substitutions, Porterfield and Hendry (1998) suggested these compounds may interact by competing for TH receptor sites and inhibit the hormone's gene expression.
Developmental toxicology; Polychlorinated biphenyls; Rats – Development; Thyroid hormones
Environmental Health and Protection | Environmental Sciences | Toxicology
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Developmental Landmarks in Offspring of Rats Exposed Singly, and in Combination to Aroclor 1016 and Levo-Thyroxine.
Bulletin of Environmental Contamination Toxicology, 67(2),