1. Perinatal BPA exposure and reproductive axis function in CD-1 mice
- Author
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Ana M. Soto, Beverly S. Rubin, Cheryl M. Schaeberle, and Nicole Acevedo
- Subjects
0301 basic medicine ,Anti-Mullerian Hormone ,Male ,medicine.medical_specialty ,endocrine system ,media_common.quotation_subject ,Fertility ,Estrous Cycle ,Gonadotropin-releasing hormone ,Biology ,Endocrine Disruptors ,Toxicology ,Article ,Gonadotropin-Releasing Hormone ,03 medical and health sciences ,Mice ,Phenols ,Pregnancy ,Internal medicine ,Follicular phase ,medicine ,Animals ,Benzhydryl Compounds ,Maternal-Fetal Exchange ,media_common ,Estrous cycle ,Neurons ,Perinatal Exposure ,urogenital system ,Estrogens ,Luteinizing Hormone ,Fecundity ,030104 developmental biology ,Endocrinology ,Female ,Luteinizing hormone ,hormones, hormone substitutes, and hormone antagonists ,Hormone - 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-Mullerian hormone (AMH) levels failed to suggest a decline in the follicular reserve at the BPA exposure levels examined.
- Published
- 2017