Over the last two decades, increasing attention has been paid to environmental toxins and their effects on the female reproductive system. Endocrine disrupting chemicals (EDCs) are exogenous substances or mixtures that can mimic the action of steroid hormones and interfere with their metabolism. Advanced glycation end products (AGEs) are proinflammatory molecules that can interact with cell surface receptors and mediate the triggering of proinflammatory pathways and oxidative stress. The purpose of this review is to explore the effects of environmental toxins exposure in the pathogenesis of both polycystic ovary syndrome (PCOS) and OC (ovarian cancer), considered separately, and also to evaluate possible neoplastic ovarian repercussion after exposure in patients diagnosed with PCOS.
Materials and methods:We searched PubMed for articles published in the English language with the use of the following MeSH search terms: "Polycystic Ovary Syndrome" and "Ovarian Cancer" combined with "endocrine disruptors". Titles and abstracts were examined and full articles that met the selection criteria were retrieved. A manual search of review articles and cross-references completed the search.Results: Extensive data from different studies collected in recent years concerning the effects of EDCs/AGEs exposure have confirmed their role in the pathophysiology of both PCOS and OC. They favour PCOS/OC development through different mechanisms that finally lead to hormonal and metabolic disruption and epigenetic modifications.Conclusions: Environmental toxin exposure in PCOS women could favour neoplastic transformation by exacerbating and potentiating some PCOS features. Further research, although difficult, is needed in order to prevent further diffusion of these substances in the environment, or at least to provide adequate information to the population considered at risk.
Several available studies have already analyzed the systemic effects of endocrine-disrupting chemicals (EDCs) on fertile woman and neonatal outcomes, but little is still known in humans about the precise mechanisms of interference of these compounds with the endometrial receptivity. There is consistent evidence that continuous and prolonged exposure to EDCs is a risk factor for reduced fertility and fecundity in women. Preliminary studies on mammalian models provide robust evidence about this issue and could help gynecologists worldwide to prevent long term injury caused by EDCs on human fertility. In this systematic review, we aimed to systematically summarize all available data about EDC effects on blastocyst endometrial implantation. We performed a systematic review using PubMed®/MEDLINE® to summarize all in vivo studies, carried out on mice models, analyzing the molecular consequences of the prolonged exposure of EDC on the implantation process. 34 studies carried out on mouse models were included. Primary effects of EDC were a reduction of the number of implantation sites and pregnancy rates, particularly after BPA and phthalate exposure. Furthermore, the endometrial expression of estrogen (ER) and progesterone receptors (PR), as well as their activation pathways, is compromised after EDC exposure. Finally, the expression of the primary endometrial markers of receptivity (such as MUC1, HOXA10, Inn and E-cadherin) after EDC contact was analyzed. In conclusion EDC deeply affect blastocyst implantation in mouse model. Several players of the implantation mechanism are strongly influenced by the exposure to different categories of EDC.
Among the different treatment options for surgical treatment of ovarian endometrioma, in our experience cystectomy appears to be the most appropriate treatment, both in terms of recurrence and pregnancy rate.
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