Effects of Bisphenol A and Diethylstilbestrol on Estrogen Receptor Expression and Male Fertility
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Abstract
Infertility is defined as a couple’s inability to conceive after one year of unpro-
tected intercourse. Male reproductive pathologies are the predominate cause
of at least 20% of cases of infertility; making male infertility is an important
issue in overall population health. Endocrine disrupting chemicals (EDCs) can
impair spermatogenesis by creating hormonal imbalances and morphological
changes. DES and BPA are both exogenous estrogens, also known as xenoestrogens.
Estrogen has an important role in fertility of males as well as females:
it has a role in the overall endocrine balance required to allow spermatogenesis.
Effects on the hypothalamic-pituitary-gonadal axis may be monitored by
assessing for upregulation of estrogen receptors α and -B (ERα and ERβ), as
well as the novel estrogen receptor g-protein coupled receptor 30 (GPR30).
Controversy surrounds the mechanisms endocrine disruption associated with
these chemicals, and whether the negative effects on fertility are relevant at
low doses, or only at high doses which are systemically toxic. Analysis of literature
associated with this ongoing research will enrich our understanding of
the molecular bases for impairment of spermatogenesis and male fertility associated
with exposure to EDCs, specifically DES and BPA. Once completed,
this study will contribute to knowledge in the fields of population health, environmental
health, and molecular genetics. With a more thorough understanding
of the impact of EDCs on fertility, it is hoped that governments will further
prevent exposure by better regulating the use of compounds such as DES and
BPA.
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Keywords
Bisphenol A, diethylstilbestrol, Endocrine Disrupting Chemicals (EDCs), xenoestrogens, male infertility, spermatogenesis, Estrogen Receptor Alpha (ERα), Estrogen Receptor Beta (ERβ), G-protein Coupled Receptor (GPR30)
