Abstract
Bisphenol A (BPA), which has previously been shown to have estrogenic activity, was examined for its effect on spermatogenesis in offspring of mice that had been exposed to BPA during gestation. BPA (0, 1, 10, or 100 mg/kg body weight) was orally administered to pregnant mice from the 10th to the 17th day of gestation, and testes of 60- and 120-day-old male offspring were removed and processed for histological analysis. The results demonstrate that prenatal exposure to BPA brings about histopathological changes in the seminiferous epithelium of testes in mouse offspring, such as loss of the luminal space of the seminiferous tubules, accumulation of amorphous material in the tubes, reduction in the number of maturating elongate spermatids, and an aberrant distribution of spermatogenic cells within the epithelium. Electron microscopy suggested that disturbed spermiogenesis is one of the reasons for the reduction in the number of elongate spermatids, and that degeneration of somatic Sertoli cells might be responsible for the aberrant distribution of spermatogenic cells within the epithelium. These data suggest that exposure to BPA during fetal life has profound effects on spermatogenesis in the testes when the offspring become adult.
