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.

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. In this disease, the entry of endometrial tissues into the peritoneal cavity causes oxidative stress through the Fenton reaction and inflammation in this site. Oxidative stress can be associated with many complications of endometriosis. In this review, an attempt has been made to discuss the effects of oxidative stress on various complications of this disease.

Background Breast cancer is one of the most common cancers. Leukemia inhibitory factor (LIF) is considered as one of the effective factors in the growth of breast cancer, and anti-leukemia inhibitory factor antibody is considered as one of the treatment options for this type of cancer. Methods Mice models of breast cancer were made with 4T1 cell line and were randomly divided into four groups. The first group included the mice that received anti-LIF (Anti LIF group). The mice in the second group received anti-LIF and doxorubicin (Anti LIF & DOX). The mice in the third group received only doxorubicin (DOX). Finally, the mice in the fourth group did not receive any intervention. 22 days after tumor induction, some of the mice were killed, and their tumor tissues, lymph nodes, and spleens were separated for evaluating P53, Caspase-3, TIM-3, LAG-3, CTLA-4, and PD-1 genes expression. The percentage of regulatory T cells and level of interferon gamma (IFN-γ) and transforming growth factor-beta (TGF-β) were evaluated. The rest of the mice were kept to check the tumor size and their survival rate. Results The proposed intervention did not have any significant effect on the tumor growth and the survival rate. However, the expression of P53 gene and Caspase-3 in the tumor tissue of the Anti LIF group had a significant enhancement. In tumor tissues and lymph nodes, the expression of T-bet, PD-1, TIM-3, and LAG-3 genes in the Anti LIF group showed a significant increase. There was no significant difference between groups in the percentage of regulatory T cells and level of IFN-γ and TGF-β. Conclusions The proposed interventions were able to have a direct effect on tumors, but no significant effect was observed on the immune system.