Introduction
Endometriosis is a hormone-inflammatory disease described by the presence of endometrial tissue outside the uterine cavity, with a prevalence of 6–10% in reproductive-age women, but as high as half when associated with chronic pelvic pain and infertility(1, 2). Several theories have been suggested to clarify the pathogenicity of endometriosis, which is delineated in Figure 1; the Sampson hypothesis presented in 1920 showed the retrograde menstruation through the fallopian tube into the peritoneal cavity principal reason for endometriosis(3, 4).
Some studies have shown endometriosis has an association with oxidative stress, characterized by a balance between the production of reactive oxygen species (ROS) and their neutralization by the antioxidant system(5-8). Oxidative stress has an essential role in the cell proliferation, inflammatory process, and the apoptosis prevention of the endometriotic cell(3, 9). Well-known inducers of oxidative stress are macrophages, erythrocytes, and apoptotic endometrial tissue, transplanted to the peritoneal cavity through retrograde menstruation(10). Fenton reaction can produce ROS 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. All of these processes result in the upregulation of the expression of multiple proinflammatory genes such as cytokines, chemokines, adhesion molecules, growth, and angiogenic factors(8). Enzymatic and non-enzymatic antioxidant defenses and permitting an overall assessment of this process(11). The present study attempts to evaluate oxidative stress’s role in the complications of endometriosis.