Investigating the Effects of Endocrine-Disrupting Chemicals/Toxicants on the Human Ovary and Its Inflammatory Signalling Pathways

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ABSTRACT The ovary is a vital organ that is sensitive and susceptible to various illnesses when disrupted. Concerns have been raised about the effect of endocrine-disrupting chemicals (EDCs) on the reproductive organs, especially the ovaries. EDCs are mainly synthetic and can be present in copious amounts in the environment, contributing to daily human exposure. Numerous studies have established a positive correlation between these chemicals and abnormal reproductive functioning. Ovary functions are undertaken through inflammatory signalling pathways – such as the cytokines; CRP; ROS; and COX-2 – which in turn alter the functionality of the organ. The purpose of this study is to investigate the effect of EDCs on the human ovary through these inflammatory signalling pathways and to determine the consequential ovarian dysfunctions. A literature review was conducted by searching the EMBASE and MEDLINE databases for in-depth studies of EDCs exposure and subsequent ovarian inflammasome effects. Relevant key terms were used, and limitations were applied to the search criteria. The literature review revealed that the precise role of the effective process of EDCs on ovarian inflammatory mediators is complicated. Experimental evidence demonstrated the ability of EDCs, for example, (BPA, HPTE, β-HCH, DDE, PBDEs, PCBs, PFASs, Phthalates) to survive in the female ovary and its component cells through the blood–follicle barrier. Furthermore, the studies presented evidence of the association between EDCs exposure and some ovarian dysfunction conditions like ovarian cancer (OC), polycystic ovarian syndrome (PCOS) and cell ageing due to its impact on the endpoint of the ovaries through the inflammation pathways specifically cytokines (TNF-α, ILs and NF-kB), CXCL12, ROS, OS and COX-2. Many of the studies assumed or associated a higher concentrated level of EDCs exposure with adverse ovarian inflammatory effects. However, these studies did not provide adequate or conclusive evidence that ovarian disruptions through the inflammatory mediators are triggered solely by EDCs exposure. Further experimental studies that test different levels of exposure in the general human population are needed in order to better understand the possible risks of EDCs on the role of ovarian inflammation.

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