Abstract:

Recurrent spontaneous abortion (RSA) has a complex and diverse etiology, and many pathophysiological mechanisms of RSA remain unknown. In the reproductive system of women, reactive oxygen species (ROS) play an important role in hormone signaling, oocyte maturation, ovarian steroidogenesis, ovulation, luteal dissolution, luteal maintenance during pregnancy, embryo implantation, blastocyst development, reproductive cell function, and luteal formation. The abnormal expression of hypoxia inducible factor-1α, iron death, exposure to trace elements and heavy metals, and other factors directly or indirectly induce oxidative stress (OS). The imbalance between oxidative and antioxidant mechanisms has a negative impact on cell proliferation and apoptosis, leading to pathological phenomena such as cellular dysfunction, decreased biological activity, immune and inflammatory activation. The maternal-fetal interface plays a role in the exchange of gases, nutrients and metabolites during pregnancy, while producing various hormones and growth factors to support the normal development of the fetus and to maintain pregnancy. Therefore, OS in maternal-fetal interface is related to the occurrence and progression of RSA.

Key words: Maternal-fetal interface, Oxidative stress, Abortion, habitual, Spermatogenesis, Signal transduction