Effects of endocrine disruptors in the development of the female reproductive tract

Abstract

Environmental agencies have identified a growing number of environmental contaminants that have endocrine disrupting activity, and these can become a major public health problem. It is suggested that endocrine disruptors could account for the higher-than-expected increase in the prevalence of some non-communicable diseases, such as obesity, diabetes, thyroid diseases, and some cancers. Several endocrine Disrupting Chemicals (EDCs), such as pesticides, bisphenol A, phthalates, dioxins, and phytoestrogens, can interact with the female reproductive system and lead to endocrine disruption. Initially, it was assumed that EDCs exert their effects by binding to hormone receptors and transcription factors, but it is currently known that they may also alter the expression of enzymes involved in the synthesis or catabolism of steroids. Biomonitoring studies have identified these compounds in adults, children, pregnant women, and fetuses. Among the diseases of the female reproductive tract associated with EDCs exposure are the following: precocious puberty, polycystic ovary syndrome, and premature ovarian failure. The different populations of the world are exposed to a great number of chemicals through different routes of infection; despite the various available studies, there is still much doubt regarding the additive effect of a mixture of EDCs with similar mechanisms of action.

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“…Several endocrine-disrupting chemicals, such as pesticides, can interact with the female reproductive system and lead to endocrine disruption (Bretveld et al, 2006;Costa et al, 2014). It has been reported that, depending on the lindane toxicity in fish, inhibition of ovarian steroidogenesis was found together with the affected reproductive system, and consequently, hormonal imbalances and significant decreases in egg production were observed (Singh et al, 1993;Ensenbach and Nagel, 1997;Mnif et al, 2011).…”

“…Mills and Chichester (2005) have pointed out that alterations in plasma sex steroid concentrations may have resulted from several different mechanisms of action, including direct effects on steroidogenic enzymes or through indirect modifications associated with altered feedback loops. Mechanisms of action of organochlorine compounds can trigger two types of response: mimicking hormonal action, as an agonistic effect, or leading to a lack of response and preventing the binding of the natural hormone, an antagonistic effect (Mnif et al, 2011;Costa et al, 2014). It was reported in other studies that organochlorine compounds did not lead to a significant change in the testosterone and estradiol (E 2 ) levels in male zebrafish, whereas the levels of estradiol and testosterone in female zebrafish had decreased (Singh et al, 1993;Chang et al, 2013).…”

Triazophos-induced oxidative stress and histomorphological changes in ovary of female Wistar rats

“…Increased atresia of ovarian follicles can be attributed to the deleterious effects of pesticides through the altered endogenous hormone levels [4,21]. Ovarian interstitial glands (IGs) formation as a result of TZ treatment may be responsible for enhanced synthesis of estradiol, as IGs have been evidenced for endogenous steroidogenesis in the ovaries [54,55].…”

A review on endocrine disruptors and their possible impacts on human health

“…This early onset of puberty may be associated with a greater 931 prevalence of many other disorders, such as insulin resistance, metabolic syndrome, breast and 932 reproductive system cancers (Costa, et al,, 2014). disease is characterized by anovulation and hyperandrogenism, and associated with higher 941 prevalence of obesity, insulin resistance and metabolic abnormalities (Costa, et al, 2014). 942…”