Journal
REPRODUCTIVE TOXICOLOGY
Volume 57, Issue -, Pages 87-99Publisher
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.reprotox.2015.05.012
Keywords
Bisphenol A; Neonatal ovaries; Mouse; Oxidative stress; Apoptosis; Germ cell nest breakdown
Categories
Funding
- NIH [PO1 ES022848]
- EPA [RD-83459301]
- Environmental Toxicology Fellowship from Interdisciplinary Environmental Toxicology Program at UIUC
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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 mu g/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. (C) 2015 Elsevier Inc. All rights reserved.
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