Polycystic ovary syndrome and environmental toxins

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Polycystic ovary syndrome and environmental toxins Aleksandra Zofia Rutkowska, Ph.D., Evanthia Diamanti-Kandarakis, M.D., Ph.D. Fertility and Sterility Volume 106, Issue 4, Pages 948-958 (September 2016) DOI: 10.1016/j.fertnstert.2016.08.031 Copyright © 2016 American Society for Reproductive Medicine Terms and Conditions

Figure 1 The possible impact of EDCs on the developing fetus. Exposure of a mother (F0 generation) to EDCs may result in direct impact of these chemicals on fetal development (F1 generation) or in EDCs-dependent disruption of the hormonal balance crucial for proper growth and differentiation of the fetus. Additionally, the impact of EDCs on epigenetic changes in fetal DNA (F1 generation) may be inherited, and adverse health effects (also PCOS phenotype) may occur not only in F1 but also in F2 and F3 generations. Fertility and Sterility 2016 106, 948-958DOI: (10.1016/j.fertnstert.2016.08.031) Copyright © 2016 American Society for Reproductive Medicine Terms and Conditions

Figure 2 Potential results of environmental factors exposure that may be linked to PCOS and its consequences. Processed, canned, and especially animal-derived foods are examples of sources of high exposure to both suspected environmental toxins, EDCs and AGEs, which may lead to endocrine, metabolic, and reproductive disruption, resulting in PCOS phenotypes and adverse health effects. Fertility and Sterility 2016 106, 948-958DOI: (10.1016/j.fertnstert.2016.08.031) Copyright © 2016 American Society for Reproductive Medicine Terms and Conditions

Figure 3 Model of BPA action on classical estrogen receptors (ERα, ERβ) and nonclassical nuclear receptors. AhRR = aryl-hydrocarbon receptor repressor; ncmE = nonclassical membrane estrogen receptors. Fertility and Sterility 2016 106, 948-958DOI: (10.1016/j.fertnstert.2016.08.031) Copyright © 2016 American Society for Reproductive Medicine Terms and Conditions

Figure 4 Potential BPA interactions with androgen synthesis and metabolism. BPA may directly impact the ovarian theca cells to secrete androgens and additionally can displace T from SHBG, thereby increasing the free androgen index and disrupting the androgen-to-estrogen balance. Androgens decrease hepatic BPA glucuronidation, leading to increased serum free BPA levels and perpetuation of BPA and androgen interactions. Fertility and Sterility 2016 106, 948-958DOI: (10.1016/j.fertnstert.2016.08.031) Copyright © 2016 American Society for Reproductive Medicine Terms and Conditions

Figure 5 PCOS and environmental toxin exposure across the life cycle. Schematic of developmental and adult windows of vulnerability to AGEs and EDCs, common environmental factors, in the pathogenesis of and pathophysiology of PCOS. Fertility and Sterility 2016 106, 948-958DOI: (10.1016/j.fertnstert.2016.08.031) Copyright © 2016 American Society for Reproductive Medicine Terms and Conditions