Perinatal BPA exposure and reproductive axis function in CD-1 mice

Reproductive Toxicology
Nicole AcevedoAna M Soto

Abstract

Perinatal Bisphenol-A (BPA) exposure reduces fertility and fecundity in mice. This study examined effects of early BPA exposure on activation of gonadotropin releasing hormone (GnRH) neurons in conjunction with a steroid-induced luteinizing hormone (LH) surge, characterized patterns of estrous cyclicity and fertility over time, and assessed the ovarian follicular reserve to further explore factors responsible for the reduced fertility we previously described in this model. The percent activated GnRH neurons was reduced in BPA-exposed females at 3-6 months, and periods of persistent proestrus were increased. These data suggest that perinatal exposure to BPA reduces GnRH neuronal activation required for the generation of the LH surge and estrous cyclicity. Assessments of anti-Müllerian hormone (AMH) levels failed to suggest a decline in the follicular reserve at the BPA exposure levels examined.

Citations

Nov 8, 2019·Toxicological Sciences : an Official Journal of the Society of Toxicology·Roberta TassinariUNKNOWN LIFE PERSUADED Project Group
Feb 23, 2019·Frontiers in Endocrinology·Beverly S RubinAna M Soto
Apr 3, 2020·Toxicological Sciences : an Official Journal of the Society of Toxicology·Isabela V SarmentoJones B Graceli
Sep 1, 2020·Environmental Pollution·Ming-Yu ZhangShun-Feng Cheng
Jan 31, 2021·Nature Reviews. Endocrinology·Ana M SotoCarlos Sonnenschein

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