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Updated: Feb 10, 2026
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Long-term Behavioral and Reproductive Consequences of Embryonic Exposure to Low-dose Toxicants
Published on: March 6, 2018
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Perinatal BPA exposure and reproductive axis function in CD-1 mice
Nicole Acevedo1, Beverly S Rubin1, Cheryl M Schaeberle1
1Department of Integrative Physiology and Pathobiology, Tufts University School of Medicine, Boston, MA, 02111, USA, USA.
Reproductive Toxicology (Elmsford, N.Y.)
|May 13, 2018
Summary
Perinatal exposure to Bisphenol-A (BPA) impairs fertility in female mice by reducing gonadotropin-releasing hormone (GnRH) neuron activation, which disrupts estrous cycles and the luteinizing hormone (LH) surge.
Area of Science:
- Endocrinology
- Reproductive Biology
- Toxicology
Background:
- Perinatal exposure to Bisphenol-A (BPA) is linked to reduced fertility and fecundity.
- Understanding the neuroendocrine mechanisms underlying BPA's effects on reproduction is crucial.
Purpose of the Study:
- To investigate the impact of early BPA exposure on gonadotropin-releasing hormone (GnRH) neuron activation.
- To characterize estrous cyclicity, fertility patterns, and ovarian reserve in BPA-exposed mice.
- To explore the factors contributing to BPA-induced reductions in fertility.
Main Methods:
- Assessed GnRH neuron activation in response to a steroid-induced luteinizing hormone (LH) surge.
- Monitored estrous cyclicity and fertility over time.
- Measured anti-Müllerian hormone (AMH) levels to evaluate ovarian follicular reserve.
Main Results:
- Reduced percentage of activated GnRH neurons observed in BPA-exposed female mice (3-6 months).
- Increased incidence of persistent proestrus in BPA-exposed mice.
- No significant decline in ovarian follicular reserve indicated by AMH levels at examined BPA exposure levels.
Conclusions:
- Perinatal BPA exposure disrupts GnRH neuronal activation, impacting LH surge generation and estrous cyclicity.
- The observed reproductive deficits in this model are likely linked to impaired GnRH neuron function.
- BPA's effects on fertility at these exposure levels do not appear to stem from a diminished ovarian reserve.
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