Chronic exposure to low dose of bisphenol A causes follicular atresia by inhibiting kisspeptin neurons in anteroventral periventricular nucleus in female mice.
Tang. Chuanfeng C; Zhang. Jia J; Liu. Peiyu P; Zhou. Yu Y; Hu. Qiaoyun Q; Zhong. Ying Y; Wang. Xiaoli X; Chen. Lei L
Key Findings
- Chronic low‑dose BPA (50 µg/kg) lengthened diestrus and lowered estrogen, LH, FSH, and GnRH levels in adult female mice.
- BPA reduced the number of antral follicles and corpora lutea, indicating impaired ovulation.
- Expression of kisspeptin in the AVPV brain region dropped with BPA exposure, but intracerebroventricular kisspeptin‑10 restored hormone levels and the LH surge.
- The BPA effect was mediated through estrogen receptor‑α (ERα), not ERβ, as shown by antagonist/agonist experiments.
Practical Outcomes
- For biohackers, the work mainly warns that chronic BPA exposure can disrupt reproductive hormones, reinforcing the need to limit BPA in diet and environment. While kisspeptin‑10 rescued the mice, it was delivered directly into the brain, a route not feasible for humans, so the finding is not yet a usable protocol. The study adds modest safety data on BPA’s endocrine impact but does not provide a ready‑to‑apply supplement or dosage for people.
Summary
A study in female mice showed that long‑term low‑dose exposure to the plastic chemical BPA messes up the brain signals (kisspeptin neurons) that control the menstrual cycle, leading to fewer mature eggs and a longer low‑fertility phase. Giving the mice a small dose of the peptide kisspeptin‑10 straight into the brain fixed the hormone drops and restored the normal LH surge, suggesting kisspeptin can counteract BPA’s harmful effect on fertility in mice.
Abstract
Bisphenol-A (BPA) is an estrogenic chemical extensively used in industrial and household applications. The present study was conducted to investigate the effect of chronic exposure to BPA on the adult female neuroendocrine system. Herein, we found that expose of adult female mice to BPA (50 μg/kg) by oral gavage for 60 days (BPA mice) prolonged diestrus and decreased serum 17β-estradiol (E2) concentration by reducing the number of antral follicles and corpora luteum. In comparison with controls, the levels of serum luteinizing hormone (LH), follicle stimulating hormone (FSH), hypothalamic gonadotrophin releasing hormone (GnRH) and the expression of kisspeptin in anteroventral periventricular nucleus (AVPV) decreased in BPA mice, which could be reversed by injecting kisspeptin-10 (i.c.v.). Treatment with BPA or estrogen receptor α (ERα) antagonist MPP, but not ERβ antagonist PHTPP inhibited E2-induced AVPV-kisspeptin expression in ovariectomized mice. Use of ERα agonist PPT rather than ERβ agonist DPN enhanced AVPV-kisspepetin expression, which decreased after treatment with BPA. The amplitude of the proestrus LH surge decreased in mice exposed to BPA, but was recovered by administering kisspeptin-10. The present study provides in vivo evidence that chronic exposure to a low dose of BPA suppressed ERα-induced activation of AVPV-kisspeptin neurons, leading to prolonged diestrus and reduced ovulation in adult female mice.
Study Information
pubmed
2020
2020-05-12T00:00:00.000Z
10.1016/j.neuro.2020.04.011
18
53