Effects of in utero exposure to 2,2',4,4',5,5'-hexachlorobiphenyl on postnatal development and thyroid function in rat offsping

Abstract

Exposure to polychlorobiphenyls (PCBs) has been reported to affect endocrine glands; however, little is known about the precise toxicological properties of individual PCBs. We determined whether prenatal exposure to 2,2′,4,4-pm,5,5′-hexachlorobiphenyl (PCB 153), a di-ortho-substituted non-coplanar congener, affects postnatal development in rat offspring. Pregnant Sprague-Dawley rats were given PCB 153 (0, 1, or 4 mg/kg/d) orally from gestational day (GD) 10 to 16, and somatic parameters and thyroid functions in offspring were examined. We found no dose-dependent changes in body weight, body length, tail length, or weight of liver, kidney, testis, seminal vesicle, prostate, ovary, relative organ weight, anogenital distance (AGD), or AGD index in offspring at 1, 3 or 9 wk of age. We observed no compound-related changes in the plasma concentrations of thyroxine (T4), tri-iodothyronine (T3) or thyroid-stimulating hormone (TSH), although there was a significant difference in T3 only in 1-wk-old males. In addition, thyroid glands from PCB 153 groups had normal T4 responses to exogenous TSH in vivo. These findings suggest that low doses of PCB 153 given prenatally (GD 10-16, 1-4 mg/kg/d) might have little effect on postnatal somatic growth or thyroid development of male and female rat offspring under the experimental conditions of the present study.