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

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2015
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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 10μg/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.
Reference Key
zhou2015bisphenolreproductive Use this key to autocite in the manuscript while using SciMatic Manuscript Manager or Thesis Manager
Authors Zhou, Changqing;Wang, Wei;Peretz, Jackye;Flaws, Jodi A;
Journal reproductive toxicology (elmsford, ny)
Year 2015
DOI
10.1016/j.reprotox.2015.05.012
URL
Keywords
bisphenol a apoptosis oxidative stress mouse germ cell nest breakdown neonatal ovaries

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