Adult exposure to BPA causes activational disruption of estrous cycle and folliculogenesis

Our society is facing a public health challenge caused by the increasing presence of endocrine disrupting chemicals (EDCs). Bisphenol A (BPA) is a widespread EDC used in the manufacture of PVC and epoxy resins. While early postnatal exposure to BPA disrupts sexual maturation andpubertal timing, , its effects on fertility after adult exposure have not yet been studied.
Female Wistar rats were exposed for 15 days to corn oil or a low (25ng/kg/d) or a high (5mg/kg/d) BPA dose subcutateouslyat 90 days of age. Animals exposed to both doses showed a disruption of the estrous cyclicity characterized by a decrease in the average time spent in proestrus. We observed a disruption on folliculogenesis characterized by a significant decrease of antral follicles and increase of atretic follicles. The exposed females showed a regular cycle one month after the last dose of BPAWe did not observe any difference in the frequency or amplitude of GnRH secretion 24h after the end of exposure.
We also observed that early postnatal exposure to BPA for 15 days disrupted estrous cycle during adulthood with a decrease in time spent in proestrus.
In conclusion, exposure to BPA neonatally or during adulthood disrupts the estrous cycle and folliculogenesis. The effects of exposure to BPA during adulthood might be independent of GnRH secretion. Moreover, the effects of early postnatal exposure to BPA are persistent while exposure to BPA during adulthood appears to causeeactivational, non persistent alteration of the oestrus cycle.