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Endometriosis is a gynecologic illness that affects women of reproductive age. The presence of endometrial tissue outside the uterine cavity distinguishes it. Pelvic discomfort and infertility plague the women who are affected. Retrograde menstruation, coelomic metaplasia, and induction theory are three main ideas that have been proposed to explain the complex etiology. Endometriosis development is also influenced by genetics and epigenetics. Recent research has focused on the role of oxidative stress, an imbalance between reactive oxygen species (ROS) and antioxidants, in the pathophysiology of endometriosis, which results in a peritoneal cavity inflammatory response. Reactive oxygen species (ROS) are inflammatory mediators that control cell growth and have harmful effects. They are formed by normal oxygen metabolism. A systematic review was conducted to understand better the many roles of oxidative stress and its role in the development of endometriosis. Iron metabolism, oxidative stress markers (in the serum, peritoneal fluid, follicular fluid, peritoneal environment, ovarian cortex, and eutopic and ectopic endometrial tissue), oxidative stress genes, endometriosis-associated infertility, and cancer development have all been studied.

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