Neonatal exposure to bisphenol A advances pubertal development in female rats

Jing Qiu1, Yanyan Sun1, Wen Sun1

  • 1Department of Integrative Medicine, Children's Hospital of Fudan University, Shanghai, China.

Insights

Neonatal exposure to Bisphenol A (BPA) significantly advanced pubertal development in female rats. Higher BPA doses led to increased hormone levels and gene expression, suggesting a dose-dependent effect on puberty onset.

Area of Science:

  • Endocrinology
  • Developmental Biology
  • Toxicology

Background:

  • Neonatal exposure to endocrine-disrupting chemicals like Bisphenol A (BPA) is a growing concern.
  • The precise impact of early-life BPA exposure on the timing of pubertal development requires further elucidation.

Purpose of the Study:

  • To investigate the effects of neonatal Bisphenol A (BPA) exposure on the pubertal development of female Sprague-Dawley rats.
  • To determine if BPA exposure influences vaginal opening, hormone levels, and key hypothalamic gene expression related to puberty.

Main Methods:

  • Female Sprague-Dawley rats received daily subcutaneous injections of varying BPA doses (0.05-10 mg·kg⁻¹·day⁻¹) or vehicle from postnatal day 1 to 10.
  • Evaluations at postnatal day 35 included day of vaginal opening (DVO), ovarian morphology, serum hormone assays, and quantitative analysis of hypothalamic Gnrh1 and Kiss1 mRNA and protein levels.

Main Results:

  • Significant advancement in DVO was observed in rats exposed to 5 and 10 mg·kg⁻¹·day⁻¹ BPA.
  • Serum hormone concentrations and hypothalamic expression of Gnrh1 and Kiss1 (both mRNA and protein) were dose-dependently increased with BPA exposure.
  • The 10 mg·kg⁻¹·day⁻¹ BPA dose group exhibited significantly upregulated hypothalamic Gnrh1 and Kiss1.

Conclusions:

  • Neonatal exposure to Bisphenol A (BPA) can significantly advance pubertal development in female rats.
  • The effects of BPA on pubertal timing appear to be dose-dependent within the tested range.
  • BPA exposure during the neonatal period may disrupt normal pubertal maturation through hormonal and neuroendocrine pathways.