Invited review
Antioxidants and female reproductive pathologies

Oxidative stress, the imbalance between pro-oxidants and antioxidants, has been evidenced in a number of female reproductive pathologies, and studies suggest its function in the etiology of many of these diseases. This review investigates the role of oxidative stress specifically in pregnancy-associated complications as well as infertility-associated complications. Placental oxidative stress has been implicated in the pathogenesis of antiphospholipid syndrome and hyperhomocysteinemia, which comprise the etiology of recurrent pregnancy loss (RPL). Oxidative stress also has been documented in relation to idiopathic RPL cases, hydaditiform mole, and preeclampsia. Oxidative stress can induce DNA damage and apoptosis, thought to be responsible for the pathophysiology of hydatidiform mole. Additionally, macrophage activation due to retrograde menstruation can induce oxidative stress, ultimately leading to endometriosis, while stimulating its proliferation. A decrease in antioxidants along with placental oxidative stress in pregnant women may activate uncontrolled lipid peroxidation, causing vascular endothelial damage resulting in preeclampsia. For women with hydrosalpinx, the presence of oxidative stress in the hydrosalpingal fluid may be the root cause of embryotoxicity. A persistent increased generation of reactive oxygen species in the peritoneal cavity seems to provide an explanation of unexplained infertility. Finally, increased oxidative stress also seems to be responsible for diminishing oocyte quality, thereby leading to oocyte aging. However, it is important to note that no widespread consensus has been reached. Continued investigation is essential because if oxidative stress is, in fact, an important part of the pathophysiology of these diseases, antioxidant supplementation may serve to reduce symptoms, restore normal function, or prevent the development of these diseases in at-risk women.