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Oxidative Stress and Its Implications in Endometrial Function

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Uterine Endometrial Function

Abstract

Oxidative stress (OS) is caused by an imbalance between the production of or exposure to reactive oxygen species (ROS) and the activity of cellular antioxidants. Mammalian cells possess multiple mechanisms to remove ROS, including the utilization of enzymatic and nonenzymatic dietary antioxidants. ROS have both physiological and pathological roles in the reproductive tract. They are key signal molecules modulating various physiological reproductive functions. However, OS is associated with a number of pregnancy complications, including preeclampsia, and reproductive disorders such as endometriosis, polycystic ovary syndrome (PCOS), and unexplained infertility. The fetomaternal interface, consisting of the maternal decidua and invading placental trophoblasts, is exposed to profound changes in oxygen tension during pregnancy. These changes at the uteroplacental interface induce a burst of intracellular ROS. Endometrial decidualization is crucial to the formation of a functional fetomaternal interface because it controls endovascular trophoblast invasion and tissue homeostasis and confers resistance to environmental stress signals, including OS. Decidualizing cells surround and encapsulate the early conceptus and their remarkable resistance to oxidative cell death ensures that the pregnancy is protected against environmental stressors. In this chapter, we discuss ROS scavenger systems in the endometrium as well as the role of OS in the pathogenesis of pregnancy complications and reproductive disorders.

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Kajihara, T., Ishihara, O., Brosens, J.J. (2016). Oxidative Stress and Its Implications in Endometrial Function. In: Kanzaki, H. (eds) Uterine Endometrial Function. Springer, Tokyo. https://doi.org/10.1007/978-4-431-55972-6_7

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