Adverse reproductive function induced by maternal BPA exposure is associated with abnormal autophagy and activating inflamation via mTOR and TLR4/NF-κB signaling pathways in female offspring rats.

Bisphenol A (BPA) can affect reproductive function, but its mechanism of reproductive toxicity is unclear, and the effect of BPA on the onset of puberty was inconsistent. The main purpose of this study is to investigate the effects of perinatal exposure to BPA on the onset of puberty and reproductive function, and its mechanism from the aspect of autophagy and inflammation in ovarian and uterus tissues of female offspring. Twenty-one pregnant SD rats were randomly divided into three groups: Control group, 1 μg/mL BPA (LBPA) and 10 μg/mL BPA group (HBPA) via drinking water from gestational day 6 to the end of lactation. After weaning, female offspring rats were fed a normal diet and drinking water for 5 weeks. The levels of E2, LH, FSH, T, and IL-6 and TNF-α, and the onset of puberty, and morphological changes in ovarian and uterine were determined in female offspring at 8 weeks. The levels of TLR4, NF-κB, PI3K/Akt/mTOR and autophagy related protein in uterine tissue were also detected. Our results indicated that perinatal exposure to BPA advanced puberty, which was associated with increased serum E2, LH and FSH levels. There was a significantly thin endometrium epithelium in HBPA group compared with control group, which may affect reproductive function. The adverse effect of perinatal BPA exposure on reproductive function maybe was associated with the activation of inflammation and abnormal autophagy via TLR4/NF-κB and mTOR signaling pathways respectively in female offspring.