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Endocr Disruptors (Austin). 2014;2(1). pii: e29088.

Gestational bisphenol A exposure and testis development.

Author information

1
Center for Nuclear Receptors and Cell Signaling; Department of Biology and Biochemistry; University of Houston, Houston, TX USA.
2
Department of Medicine; Immunobiology Program; University of Vermont; Burlington, VT USA.
3
Department of Medicine; Immunobiology Program; University of Vermont; Burlington, VT USA ; Department of Pathology; University of Vermont; Burlington, VT USA.

Abstract

Virtually all humans are exposed to bisphenol A (BPA). Since BPA can act as a ligand for estrogen receptors, potential hazardous effects of BPA should be evaluated in the context of endogenous estrogenic hormones. Because estrogen is metabolized in the placenta, developing fetuses are normally exposed to very low endogenous estrogen levels. BPA, on the other hand, passes through the placenta and might have distinct adverse consequences during the sensitive stages of fetal development. Testicular gametogenesis and steroidogenesis begin early during fetal development. These processes are sensitive to estrogens and play a role in determining the number of germ stem cells, sperm count, and male hormone levels in adulthood. Although studies have shown a correlation between BPA exposure and perturbed reproduction, a clear consensus has yet to be established as to whether current human gestational BPA exposure results in direct adverse effects on male genital development and reproduction. However, studies in animals and in vitro have provided direct evidence for the ability of BPA exposure to influence male reproductive development. This review discusses the current knowledge of potential effects of BPA exposure on male reproductive health and whether gestational exposure adversely affects testis development.

KEYWORDS:

bisphenol A; estrogen receptors; reproductive toxicology; testis development

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