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Review
. 2019;17(12):1109-1132.
doi: 10.2174/1570159X17666190726112101.

Neuro-toxic and Reproductive Effects of BPA

Antonietta Santoro  1 , Rosanna Chianese  2 , Jacopo Troisi  1   3   4 , Sean Richards  5   6 , Stefania Lucia Nori  1 , Silvia Fasano  2 , Maurizio Guida  1   3   4 , Elizabeth Plunk  5 , Andrea Viggiano  1 , Riccardo Pierantoni  2 , Rosaria Meccariello  7
Affiliations
Review

Neuro-toxic and Reproductive Effects of BPA

Antonietta Santoro et al. Curr Neuropharmacol. 2019.

Abstract

Background: Bisphenol A (BPA) is one of the highest volume chemicals produced worldwide. It has recognized activity as an endocrine-disrupting chemical and has suspected roles as a neurological and reproductive toxicant. It interferes in steroid signaling, induces oxidative stress, and affects gene expression epigenetically. Gestational, perinatal and neonatal exposures to BPA affect developmental processes, including brain development and gametogenesis, with consequences on brain functions, behavior, and fertility.

Methods: This review critically analyzes recent findings on the neuro-toxic and reproductive effects of BPA (and its analogues), with focus on neuronal differentiation, synaptic plasticity, glia and microglia activity, cognitive functions, and the central and local control of reproduction.

Results: BPA has potential human health hazard associated with gestational, peri- and neonatal exposure. Beginning with BPA's disposition, this review summarizes recent findings on the neurotoxicity of BPA and its analogues, on neuronal differentiation, synaptic plasticity, neuroinflammation, neuro-degeneration, and impairment of cognitive abilities. Furthermore, it reports the recent findings on the activity of BPA along the HPG axis, effects on the hypothalamic Gonadotropin Releasing Hormone (GnRH), and the associated effects on reproduction in both sexes and successful pregnancy.

Conclusion: BPA and its analogues impair neuronal activity, HPG axis function, reproduction, and fertility. Contrasting results have emerged in animal models and human. Thus, further studies are needed to better define their safety levels. This review offers new insights on these issues with the aim to find the "fil rouge", if any, that characterize BPA's mechanism of action with outcomes on neuronal function and reproduction.

Keywords: BPA; GnRH; HPG axis; Kiss1; epigenetics; hypothalamus; neuroinflammation; neuronal differentiation; reproduction; synaptic plasticity..

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Figures

Fig. (1)
Fig. (1)
The chemical structure of BPA, BPB, BPF, BPS and BPAF.
Fig. (2)
Fig. (2)
Schematic overview of the main effects of BPA in rodent brain. E2, 17β-estradiol; NPCs, Neuroepithelial Progenitor Cells. (A higher resolution / colour version of this figure is available in the electronic copy of the article).
Fig. (3)
Fig. (3)
The targets of BPA along the HPG axis and the possible interplay with metabolic and environmental factors. (A higher resolution / colour version of this figure is available in the electronic copy of the article).
See this image and copyright information in PMC

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