{"title":"Endocrine disruption and female reproductive health: Implications on cross-talk between endocrine and autocrine/paracrine axes in the ovary","authors":"Subhasri Biswas, U. Mukherjee, S. Maitra","doi":"10.25259/jrhm_11_2020","DOIUrl":null,"url":null,"abstract":"Female reproduction is a blend of neuroendocrine, endocrine, and autocrine/paracrine factors that maintain the appropriate ovarian micro-environment. The growing urbanization prompted exposure to a myriad of environmental toxins carrying the ability to interfere with reproductive processes governed by endogenous hormones, making reproductive health a major global concern. These environmental anthropogenic contaminants, popularly termed as endocrine-disrupting chemicals (EDCs), can disrupt the ovarian homeostasis leading to serious perturbations, namely, anovulation, infertility, estrogen deficiency, and premature ovarian failure. Although gonadotropin action, biosynthesis of gonadal steroids vis-a-vis growth factors comprise the essential modulators within the ovary, the redox balance along with inflammatory and cell death response can dramatically influence the framework of ovarian dynamics; however, details of which remain relatively less understood. The present overview provides an update on candidates (endocrines and autocrine/paracrine) of oogenesis, and the potential impact of EDCs on diverse intra-ovarian entities including but not limited to gonadotropin action, steroidogenic potential, expression of growth factors, and modulation of maturational competence. Moreover, the relative importance of free radical-induced stress, inflammation, and elevated cell death (follicular atresia), in the regulation of ovarian functions and how these intricate yet conjoined mechanisms may alter the reproductive performance of a female will be an issue of discussion.","PeriodicalId":91915,"journal":{"name":"Journal of reproductive health and medicine","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"2020-11-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"1","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of reproductive health and medicine","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.25259/jrhm_11_2020","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 1
Abstract
Female reproduction is a blend of neuroendocrine, endocrine, and autocrine/paracrine factors that maintain the appropriate ovarian micro-environment. The growing urbanization prompted exposure to a myriad of environmental toxins carrying the ability to interfere with reproductive processes governed by endogenous hormones, making reproductive health a major global concern. These environmental anthropogenic contaminants, popularly termed as endocrine-disrupting chemicals (EDCs), can disrupt the ovarian homeostasis leading to serious perturbations, namely, anovulation, infertility, estrogen deficiency, and premature ovarian failure. Although gonadotropin action, biosynthesis of gonadal steroids vis-a-vis growth factors comprise the essential modulators within the ovary, the redox balance along with inflammatory and cell death response can dramatically influence the framework of ovarian dynamics; however, details of which remain relatively less understood. The present overview provides an update on candidates (endocrines and autocrine/paracrine) of oogenesis, and the potential impact of EDCs on diverse intra-ovarian entities including but not limited to gonadotropin action, steroidogenic potential, expression of growth factors, and modulation of maturational competence. Moreover, the relative importance of free radical-induced stress, inflammation, and elevated cell death (follicular atresia), in the regulation of ovarian functions and how these intricate yet conjoined mechanisms may alter the reproductive performance of a female will be an issue of discussion.