Developmental exposure to pentachlorophenol affects the expression of thyroid hormone receptor β1 and synapsin I in brain, resulting in thyroid function vulnerability in rats

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Abstract

Pentachlorophenol (PCP), a component of biocides and a contaminant in diverse tissue samples from humans from various geographic areas, disrupts regulatory effects of thyroid hormones. Here we examined the effects of developmental exposure of rats to PCP on various aspects of brain development, male reproductive function, and adrenal function, all of which are under thyroid hormones regulation. PCP was administered to dams and their offspring via drinking water (6.6 mg l−1) during gestation and lactation. Tissue samples were obtained from dams, 3-week-old weanling pups, and 12-week-old pups. Gene expressions of thyroid hormone receptor β1 and synapsin I, factors that promote brain growth, was increased in the cerebral cortex of PCP-treated weanling females, whereas plasma concentrations of total thyroxine were decreased in dams and weanling pups, and plasma thyroid-stimulating hormone concentrations were higher in PCP-treated weanling males. PCP caused a decrease in plasma corticosterone concentrations in 12-week-old female rats, but not in male rats or weanling females. PCP-treated male pups had significantly increased testis weight at 12 week of age. No overt signs of toxicity were noted throughout this study. Our results show that PCP exposure during development causes thyroid function vulnerability, testicular hypertrophy in adults, and aberrations of brain gene expression.

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