Bisphenol A exposure inhibits germ cell nest breakdown by reducing apoptosis in cultured neonatal mouse ovaries

Changqing Zhou, Wei Wang, Jackye Peretz, Jodi A. Flaws

Research output: Contribution to journalArticlepeer-review

Abstract

Bisphenol A is a known endocrine disrupting chemical and reproductive toxicant. Previous studies indicate that in utero BPA exposure increases the percentage of germ cells in nests and decreases the percentage of primordial follicles. However, the mechanism by which BPA affects germ cell nest breakdown is unknown. Thus, we hypothesized that BPA inhibits germ cell nest breakdown by interfering with oxidative stress and apoptosis pathways. To test our hypothesis, ovaries from newborn mice were collected and cultured with vehicle (dimethyl sulfoxide, DMSO) or different doses of BPA (0.1, 1, 5, and 10. μg/mL). Ovaries then were subjected to histological evaluation of germ cell nests and primordial follicles or to measurements of factors that regulate oxidative stress and apoptosis. Our results indicate that in vitro BPA exposure significantly inhibits germ cell nest breakdown by altering the expression of key ovarian apoptotic genes, but not by interfering with the oxidative stress pathway.

Original languageEnglish (US)
Pages (from-to)87-99
Number of pages13
JournalReproductive Toxicology
Volume57
DOIs
StatePublished - Nov 1 2015

Keywords

  • Apoptosis
  • Bisphenol A
  • Germ cell nest breakdown
  • Mouse
  • Neonatal ovaries
  • Oxidative stress

ASJC Scopus subject areas

  • Toxicology

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