Maternal exposure to bisphenol A during pregnancy interferes ovaries development of F1 female mice.

This study was conducted to investigate the effects of maternal exposure bisphenol A (BPA) on ovaries development of F1 female mice. The BPA exposure model of pregnant mice was prepared by intragastric administration of BPA at the doses of 0, 2.5, 5, 10, 20, 40 mg kg-1 d-1 at gestation day (GD) 0.5-17.5. The ovarian index of the offspring mice was calculated at postnatal day (PND) 21 and PND 56. The results showed that BPA at 5 mg/kg, 10 mg/kg, 20 mg/kg and 40 mg/kg significantly increased the abortion rate of the pregnant mice, and each dose of BPA significantly reduced the survival rate of the pups (P < 0.01 or P < 0.05). Besides, there was a non-monotonic dose-response relationship between serum hormone, ovarian receptor levels and BPA in F1 females at both PND 21 and 56. BPA increased the ovarian/uterine index in F1 females at both PND 21 and 56, increased the mRNA relative transcript levels of ovarian ERα, PgR and DNA methyltransferase (DNMT) in F1 females at PND 21, while decreased at PND 56 (P < 0.01 or P < 0.05). BPA also increased the relative expression of caspase-7, caspase-9, bax, inhibited the relative expression of bcl-2 in F1 females at both PND 21 and 56, and increased the apoptosis rate in the ovaries in F1 mice at PND 56 (P < 0.01). The number of follicles in the ovary was increased in F1 females at PND 21, and the ovaries were significantly atrophied when sexual maturity (PND 56). Our results indicated that BPA could disturb the contents of DNMT and make reproductive injury to the offspring females.