Abstract

Background: Endometriosis is a chronic and relatively common disease in women of childbearing age. Complications of this disease include a wide range of disorders. The cause of this disease is not known for sure, but several hypotheses have been proposed for it. Aim: In this review, an attempt has been made to discuss the effects of oxidative stress on various complications of endometriosis. Content: In endometriosis, the entry of endometrial tissues into the peritoneal cavity causes oxidative stress through the Fenton reaction and inflammation in this site. Fenton reaction can produce reactive oxygen species through a catalytic form of iron. This process can provoke inflammatory responses and oxidative injury. As a result, the activity of macrophages and expression of nuclear factor-kappa B increase. Oxidative stress can be associated with many complications of endometriosis. It has been reported that in the peritoneal fluid of endometriosis patients, there are activated macrophages, growth factors, and high concentrations of cytokines. These conditions act as a toxic to embryo survival and sperm function. Implications: Novel therapeutic strategies must regulate intracellular ROS signaling to inhibit the adverse effects of ROS-induced endometriosis-promoting events. According to features of antioxidants, they may inhibit early events of the development of endometriosis. © 2022 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.