Oxidative Stress and the Endometriosis

Researches did not report a definitive conclusion about the association between OS and endometriosis. Endometriosis may result in infertility due to mechanical blockage of the sperm-egg union by endometriomata, or adhesions, or pelvic anatomy malformations.

Peritoneal fluid of women with endometriosis has been found to be increased in size and contains high concentration of activated macrophages, cytokines, and pros-taglandins. Activated macrophage may be responsible for increased production of ROS. Alpay et al. [204] suggest that ROS may enhance growth and adhesion of endometrial cells in the peritoneal cavity, promoting endometriosis adhesions and infertility. In addition, Murphy et al. [205] reported a correlation between high level of ROS produced by peritoneal macrophages and LPO in endometriosis patients, whereas Jackson et al. [206] reported a weak association between LPO and endometriosis, and other researchers reported no association [175].

High levels of NO generated by peritoneal macrophages were detected. NO may change the composition of the peritoneal fluid which may affect the processes of ovulation, gamete transport, sperm-oocyte interaction, fertilization, and early embryonic development [207]. Many studies reported that peritoneal fluid has a reduced TAC and individual antioxidant enzymes such as SOD, which reflect a weak defense ability [208] .

A significant increase of ROS in the oviduct fluid could result in oxidative damage to the oocyte and spermatozoa viability and the process of fertilization and embryo transport in the oviduct. This increase in ROS may affect the spermatozoa plasma membrane and the acrosome causing inability to bind and penetrate the oocyte, respectively [204] .

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