Reproductive biomedicine online · 2025
Bisphenol A exposure induces polycystic ovarian syndrome phenotype B and reduces fertility in adolescent female rats.
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Zhang Wenjing, Huang Ruofan, Chen Jiahao, Ren Lulu, Wang Lei, Chen Qionghua, Zhou Weidong
Аннотация
RESEARCH QUESTION: Does adolescent exposure to bisphenol A (BPA) induce polycystic ovary syndrome (PCOS)-like phenotypes in female rats?
DESIGN: Adolescent Sprague-Dawley rats (6-8 weeks old) were administered BPA (50 mg/kg body weight) in corn oil, or corn oil vehicle alone, daily for 10 weeks via gastric gavage. The rats' oestrous cycle was consistently evaluated from the initiation of BPA exposure, and observation was continued for 21 days after the exposure had ended. Serum sex hormone concentrations, blood glucose metabolism, ovarian morphology and fertility were investigated.
RESULTS: Adolescent exposure to BPA resulted in irregular oestrous cycles and abnormal ovulation in female rats. Compared with the control group, BPA exposure increased the serum concentrations of testosterone, LH, insulin and glucagon, but reduced the serum concentrations of oestradiol, prolactin, sex hormone-binding globulin and anti-Müllerian hormone. BPA exposure during adolescence caused ovarian atrophy in the rats in adulthood but did not lead to polycystic changes in the ovaries. Moreover, female rats exposed to BPA showed a significant decrease in terms of litter number and weight.
CONCLUSIONS: Exposure of adolescent female rats to BPA induced a PCOS-like syndrome that was similar to clinical subtype B of PCOS in adulthood and led to a marked decline in fertility. The findings further extend the research on endocrine-disrupting chemicals in reproduction, which would help to shed light on the pathogenesis of PCOS.
DESIGN: Adolescent Sprague-Dawley rats (6-8 weeks old) were administered BPA (50 mg/kg body weight) in corn oil, or corn oil vehicle alone, daily for 10 weeks via gastric gavage. The rats' oestrous cycle was consistently evaluated from the initiation of BPA exposure, and observation was continued for 21 days after the exposure had ended. Serum sex hormone concentrations, blood glucose metabolism, ovarian morphology and fertility were investigated.
RESULTS: Adolescent exposure to BPA resulted in irregular oestrous cycles and abnormal ovulation in female rats. Compared with the control group, BPA exposure increased the serum concentrations of testosterone, LH, insulin and glucagon, but reduced the serum concentrations of oestradiol, prolactin, sex hormone-binding globulin and anti-Müllerian hormone. BPA exposure during adolescence caused ovarian atrophy in the rats in adulthood but did not lead to polycystic changes in the ovaries. Moreover, female rats exposed to BPA showed a significant decrease in terms of litter number and weight.
CONCLUSIONS: Exposure of adolescent female rats to BPA induced a PCOS-like syndrome that was similar to clinical subtype B of PCOS in adulthood and led to a marked decline in fertility. The findings further extend the research on endocrine-disrupting chemicals in reproduction, which would help to shed light on the pathogenesis of PCOS.