Gestational and lactational exposure to heptachlor does not alter reproductive system development in rats.

Abstract

Like other organochlorine insecticides, heptachlor is lipophilic and accumulates in fatty tissues. Earlier studies suggested that in utero exposure to heptachlor decreased fertility in the offspring; neonatal exposure to the closely related insecticide chlordane reportedly delayed puberty and disrupted estrous cycling in females. We hypothesized that in utero and lactational exposure to heptachlor would disrupt the development of the reproductive system in males and females, resulting in altered timing of puberty and abnormal gonadal histology and reproductive hormone levels. Timed pregnant Sprague-Dawley rats were treated by oral gavage with heptachlor in corn oil at doses of 0.5 and 5.0 mg/kg or an equivalent volume of corn oil alone daily from gestational day 8 through post-natal day (PND) 21, the day of weaning (n = 7-8/group). Litters were standardized to 4 males and 4 females on the day of birth. Two of the dams in the 5.0 mg/kg/d group died. Pups in the highest dose group weighed significantly less than those in the other 2 groups on PND 0. All but 1 litter of the 5.0 mg/kg/d group died within the first 4 post-natal days. Age at eye opening was delayed with increasing heptachlor dose. There was no effect of treatment on pup weight gain in the surviving litters, on anogenital distance, age at puberty, nipple retention past the infantile period in males, estrous cycling, serum sex steroid concentrations, reproductive organ weights, or testicular or ovarian histology. These results suggest that heptachlor exposure during gestation and lactation does not disrupt development of the reproductive system in rats.