Bisphenol A-induced polycystic ovary syndrome (PCOS) with hormonal and metabolic implications in rats.

There is a rising incidence of polycystic ovary syndrome (PCOS) cases worldwide in women of reproductive age due to environmental factors. We evaluated the effect of an environmental estrogen, bisphenol A (BPA) for its reprotoxicity regarding the induction of PCOS in rats and also assessed its hormonal and metabolic implications. There was 66.6 % and 50 % disorder, in the estrus cycle at low (50 µg/kg) and high (500 µg/kg) doses of BPA, respectively. While animals treated with the positive control (dehydroepiandrosterone, DHEA at 6 mg/100 g) caused 100 % disorder. Cystic and atretic follicles along with two corpora lutea were found in the low dose group. However, no corpus luteum was found in the high dose group. Furthermore, hyperplasia and hypertrophy were found in the myometrium, endometrium, and luminal epithelium of the uterus of the low dose and DHEA groups. Additionally, 17β estradiol, progesterone, DHEA, androstenedione, testosterone, dihydrotestosterone (DHT), dehydroepiandrosterone sulphate (DHEAS), antimullerian hormone (AMH), ratio of LH/FSH and testosterone/DHT were increased significantly (P < 0.01) in BPA groups. A significantly higher TSH (P < 0.01) indicates hypothyroidism. Furthermore, hyperglycemia, hyperinsulinemia, HOMA-IR, and HOMAβ indicate insulin resistance in the low-dose group. Thus, the low dose of BPA was found to be more potent as compared to the higher dose in defining the hyperandrogenic state. Our study revealed that BPA may not only be a causative factor in the induction of PCOS but also has metabolic implications bearing on its estrogenic nature.