# Environmental Pollution and Oxidative Stress: Health Effects During Pregnancy: A Review
## 4 Oxidative Stress and Reproductive System Complications  
Endometriosis is a harmless, estrogen-reliant, constant gynecological problem, the principal element of which is the presence of endometrial tissue outside the uterine hole. Endometriosis influences 6-10% of mature conceptive women and is joined by pelvic agony as well as fruitlessness [43]. The most well-known factor that can cause endometriosis is retrograde period, but different elements are viewed as potential causes like diminished insusceptible reaction, hereditary inclination, and variables that cause aggravation [45]. Oxidative pressure is considered as an extra element, which is possibly engaged with the pathophysiology of endometriosis [52]. ROS is likely a causative component of infertility related to the disease [53]. Also, it assumes a significant part in managing the outflow of qualities encoding immunomodulators, cytokines, and cell attachment atoms engaged with the pathogenesis of endometriosis [54]. The expanded creation of hydroxyl and different revolutionaries during endometriosis is because of the enactment of the safe framework [55]. Be that as it may, different examinations on the immediate estimation of ROS, NO, lipid peroxidation, and absolute cancer prevention agent status did not identify huge contrasts in the peritoneal liquid of healthy women and women with the disease [56; 57]. This can be most likely due to the capacity to identify only stable controls or oxidative stress products during endometriosis or even to the localized appearance of oxidative stress. As mentioned earlier, one factor that can cause endometriosis is retrograde menstruation. This pathological condition is associated with the transport of pro-oxidating factors to the peritoneal cavity, such as heme and iron, as well as apoptotic endometrial cells, which are oxidative stress inducers. However, elevated levels of iron in the peritoneal fluid of patients with endometriosis are not always associated with elevated levels of lipid peroxidation and are therefore not always involved in the catalysis of free radical reactions. Normally, during various phases of the menstrual cycle in women, changes are observed in the expression of antioxidant enzymes such as glutathione peroxidase (GPX) on the surface and the glandular epithelium of the endometrium. On the contrary, in cases of endometriosis, no similar changes are observed. Abnormal GPX expression suggests a pathological role in these cases [58]. During endometriosis, there is often an increased expression of superoxide dismutase (SOD) and in particular Cu-Zn-SOD and Mn-SOD, suggesting the important role that superoxide plays in infertility observed during endometriosis [59]. Several studies have shown controversial effects of oxidative stress biomarkers in relation to endometriosis. More specifically, some studies have shown increased levels of oxidative stress in the peritoneal fluid or circulation of patients with endometriosis, while others have not shown similar results [60; 61; 62]. Among the biomarkers of oxidative stress are lipid peroxidation products such as 4-hydroxy-2-nonenal (HNE), malondialdehydehyde (MDA), and F2-isoprostanes. Past works have shown expanded degrees of F2-isoprostanes in the peritoneal liquid and plasma of patients with endometriosis contrasted with healthy people [47]. Another biomarker of stress that has been displayed to portray the event of endometriosis is HSP70. All the more explicitly, overexpression of HSP70B has been seen alongside ROS overflow [63], which prompts the statement of provocative cytokines TNF-alpha, IL-1 beta, and IL-6 in macrophages, which eventually prompts the advancement of endometriosis [64]. Notwithstanding HSP70B, one more protein in the HSP70 family, HSP70b, has been accounted for to increase dissemination in patients with endometriosis [65].