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.