Abstract
Endocrine-disrupting chemicals (EDCs) are increasingly prevalent in the environment and the evidence demonstrates that they affect reproductive health, has been accumulating for the last few decades. In this review of recent literature, we present evidence of the effects of estrogen-mimicking EDCs on female reproductive health especially the ovaries and uteri. As representative EDCs, data from studies with a pharmaceutical estrogen, diethylstilbestrol (DES), an organochlorine pesticide methoxychlor (MXC), a phytoestrogen (genistein), and a chemical used in plastics, bisphenol a (BPA) have been presented. We also discuss the effects of a commonly found plasticizer in the environment, a phthalate (DEHP), even though it is not a typical estrogenic EDC. Collectively, these studies show that exposures during fetal and neonatal periods cause developmental reprogramming leading to adult reproductive disease. Puberty, estrous cyclicity, ovarian follicular development, and uterine functions are all affected by exposure to these EDCs. Evidence that epigenetic modifications are involved in the progression to adult disease is also presented.
Highlights
It is well known that toxic contaminants in air, water, and agricultural produce have contributed to exposure to mutagens that cause numerous health problems including cancers [1 - 3]
Neonatal estradiol or DES exposures induce multioocyte follicles (MOFs) and inhibit activin levels in the ovary [62]. These results suggest that the paracrine systems that control the primordial follicle formation process can be influenced by estrogenic endocrine-disrupting chemicals (EDCs)
A salient point to be noted regarding these processes is that the ovary is a hormone-responsive tissue and contains follicles at every stage of development that are highly dynamic and require temporal and cell-specific and stage dependent regulation of numerous genes, which could be controlled by epigenetic mechanisms
Summary
It is well known that toxic contaminants in air, water, and agricultural produce have contributed to exposure to mutagens that cause numerous health problems including cancers [1 - 3]. Neonatal estradiol or DES exposures induce MOFs and inhibit activin levels in the ovary [62] These results suggest that the paracrine systems that control the primordial follicle formation process can be influenced by estrogenic EDCs. The oocyte-derived FOXO3 is a major suppressor of primordial to primary follicle transition [63]. A salient point to be noted regarding these processes is that the ovary is a hormone-responsive tissue and contains follicles at every stage of development that are highly dynamic and require temporal and cell-specific and stage dependent regulation of numerous genes, which could be controlled by epigenetic mechanisms They can be affected by developmental exposures to EDCs making the ovary a unique target for EDCs for epigenetic modulation
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