Neonatal exposure to bisphenol A advances pubertal development in female rats

Abstract

Neonatal exposure to bisphenol A (BPA) is hypothesized to advance pubertal development. However, the effects of neonatal BPA exposure on pubertal development has not been described. In this study, female Sprague-Dawley rats were exposed to 0.05, 0.5, 5, or 10 mg·kg −1 ·day −1 BPA, or corn oil vehicle alone from postnatal day 1 (PND1) to PND10 via subcutaneous injection. We evaluated day of vaginal opening (DVO), ovarian morphology, serum hormone concentrations, and hypothalamic expression of Gnrh1 and Kiss1 in female rats at PND35. DVO was significantly advanced in rats exposed to 5 and 10 mg·kg −1 ·day −1 BPA. Serum hormone concentrations increased as BPA dose increased. Additionally, hypothalamic Gnrh1 and Kiss1 expression were increased with BPA exposure; rats exposed to 10 mg·kg −1 ·day −1 BPA had significantly upregulated hypothalamic Gnrh1 and Kiss1 expressions in terms of both messenger RNA and protein levels. Our results suggest that exposure to a 10 mg·kg −1 ·day −1 dose of BPA might advance pubertal development significantly. In addition, within the range of 0 to 10 mg·kg −1 ·day −1 , neonatal exposure to BPA may affect pubertal development in a dose-dependent manner.

Bisfenol a y efectos de disrupción endocrina en humanos y animales: Revisión sistemática

“…Con relación a esto, existen varios estudios que han resaltado la implicación del BPA en la infertilidad. En hombres, se ha et al, 2017; Morales et al, 2018;Qiu et al, 2020;Spörndly-Nees et al, 2018;Zhang et al, 2020;Zhang et al, 2018;Zhang et al, 2017).…”

“…período fetal y neonatal, y por tanto inducir efectos nocivos a largo plazo en el feto y el recién nacido (Murata & Kang, 2018). A nivel celular, el BPA mimetiza la acción hormonal e interfiere en vías de señalización involucradas en procesos como carcinogénesis, toxicidad reproductiva, respuesta inflamatoria o inmunitaria, cerebro y sistema nervioso (Chen et al, 2018;Eker et al, 2021;Qiu et al, 2020;Salehpour et al, 2020;Wen et al, 2020).…”

Review on bisphenol A and the risk of polycystic ovarian syndrome: an insight from endocrine and gene expression

“…On the other hand, neonatal exposure to BPA in female Sprague Dawley rats is seen to cause an upregulation of KISS1 and GNRH1 genes. Kisspeptin regulates the surge in gonadotropin levels during the initiation of female puberty and its activation by the neonatal BPA exposure shows that it can affect pubertal development (Qiu et al 2020). This observation is also seen in a study conducted by Xi et al (2011) on CD-1 mice, perinatal exposure to BPA causes upregulation of KISS1 mRNA and GNRH mRNA in adults, which in turn causes alteration in the gene expression of gonadotropins (FSHB, LHB) and their receptors (FSHR, LHCGR ).…”

“…A study conducted by Qiu et al (2020) observes normal ovarian morphology and follicular development, in adult rats that were neonatally exposed to BPA. Since the time of exposure plays a huge role in the development of effects, this could contribute to the difference in results (Qiu et al 2020).…”

Impact of Environmentally Relevant Concentrations of Bisphenol A (BPA) on the Gene Expression Profile in an In Vitro Model of the Normal Human Ovary

“…Over the past decade, there have been a number of studies pointing toward the adverse effects of BPA on female reproductive tissues in both human and animal studies. For example, BPA was found to exert effects on normal ovaries, with oocyte abnormalities noted in adult mice exposed to BPA [22], whereas rats exposed to BPA (10 mg•kg −1 •day −1 ) accelerated pubertal development [23]. BPA also disrupts and increases oocyte degeneration in human oocytes and meiotic maturation [24].…”