Implication of oxidative stress in the development of complications of pregnancy and postpartum


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Abstract

The review considers the role of oxidative stress in the physiological and pathological course of pregnancy and postpartum. It underlines the importance of oxidative balance for the normal course of pregnancy, the development of an embryo, and the monitoring of inflammatory cytokines.
Impaired placentation makes a considerable contribution to the pathogenesis of miscarriages and preeclampsia. Placental tissue oxidative stress induced by the excessive production of active oxygen forms (AOF) is a common pathophysiological mechanism in early pregnancy loss of varying etiologies. It is considered to be a key intermediate step in the pathogenesis of preeclampsia.
The presence of proinflammatory cytokines and AOF at high concentrations leads to the degradation of lipids, proteins, and nucleic acids. Modified proteins change their antigenicity and are involved in the immune reactions resulting in inflammatory and/or autoimmune lesions.
Postpartum is accompanied by lower oxidative stress than is pregnancy. Postpartum infectious complications are associated with the significant activation of leukocytes and the increases in the production of proinflammatory cytokines and in the generation of AOF by puerperal cells.

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