Abstract
Several studies have highlighted the negative effects of bisphenol A (BPA), a chemical compound with estrogenic activity, on reproductive health. To elucidate the impact of BPA on spermatogenesis' establishment and mechanisms of action of BPA and 17β-estradiol (E2), as both can be found in the environment, we exposed rats to BPA (50μg/kg bw/day of BPA), E2 (20μg/kg bw/day of E2) and BPA+E2 from 15 to 30days post-partum. Histological and gene expression studies revealed that BPA and BPA+E2 exposures promoted spermatogenesis establishment whereas E2 alone delayed it. Then, a decrease in gene expression of blood-testis-barrier (BTB) proteins was observed in all treated groups. Therefore, our study has demonstrated a differential effect of BPA and E2 exposures on spermatogenesis establishment in prepubertal rats and a deleterious effect of these chemicals on BTB establishment. Thus, the effects of BPA seem to be mediated by receptors other than estrogen receptors.