Female reproductive function depends upon the exquisite control of ovarian steroidogenesis that enables folliculogenesis, ovulation, and pregnancy. These mechanisms are set during fetal and/or neonatal development and undergo phases of differentiation throughout pre-and post-pubescent life. Ovarian development and function are collectively regulated by a host of endogenous growth factors, cytokines, gonadotropins, and steroid hormones as well as exogenous factors such as nutrients and environmental agents. Endocrine disruptors represent one class of environmental agent that can impact female fertility by altering ovarian development and function, purportedly through estrogenic, anti-estrogenic, and/or anti-androgenic effects. This review discusses ovarian development and function and how these processes are affected by some of the known estrogenic and anti-androgenic endocrine disruptors. Recent information suggests not only that exposure to endocrine disruptors during the developmental period causes reproductive abnormalities in adult life but also that these abnormalities are transgenerational. This latter finding adds another level of importance for identifying and understanding the mechanisms of action of these agents.
1-IntroductionThe primary function of an adult ovary is to produce the steroid and protein hormones needed to support (1) the development and maturation of ovarian follicles (i.e., folliculogenesis) including oocytes, (2) ovulation, and (3) the initiation and maintenance of pregnancy in mammals. In order for this to collectively occur, the secretion of ovarian hormones is tightly regulated by the neuroendocrine system and is locally controlled by many intraovarian feedback mechanisms (reviewed in [1]).Two major developmental events within the ovary are follicular assembly (i.e., the formation of primordial follicles) and the primordial-to-primary follicle transition (the "initial" recruitment) [1]. The initial phase of folliculogenesis is regulated by paracrine growth factors Correspondence: Dr. Mehmet Uzumcu, Department of Animal Sciences, School of Environmental and Biological Sciences, Rutgers, The State University of New Jersey, 84 Lipman Drive, New Brunswick, NJ Supported by NIH grant R21 ES013854-01A1 (MU) and funds from Robert Wood Johnson Medical School-UMDNJ (RZ).Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.
NIH Public Access Author ManuscriptReprod Toxicol. Author manuscript; available in PMC 2007 August 21.
Published in final edited form as:Reprod Toxicol. 2007 ; 23(3): 337-352.
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