Oxidative Stress in Preeclampsia and Preterm Newborn

Oxidative stress, resulting from an imbalance between reactive species (RS) and antioxidants, plays a crucial role in the pathophysiology of preeclampsia, a pregnancy-related clinical syndrome affecting both mother and fetus. Preeclampsia is characterized by new-onset hypertension and additional features such as proteinuria, maternal organ dysfunction, and uteroplacental dysfunction. The placenta, as the primary source of RS, experiences oxidative stress throughout pregnancy, particularly in the latter half. Deficient remodeling of uterine spiral arteries by invasive extravillous trophoblasts is associated with early-onset preeclampsia, leading to placental ischemia-reperfusion and subsequent oxidative stress. Late-onset preeclampsia arises due to an inadequate response of the dysfunctional maternal endothelium to oxidative stress. Preeclampsia also disrupts ATPase activities, particularly Na,K-ATPase and plasma membrane Ca-ATPase, in maternal and fetal tissues, contributing to altered ion homeostasis and cellular dysfunction. Fetuses and newborns are particularly susceptible to oxidative stress due to heightened free radical (FR) production, inadequate antioxidant protection, and rapidly developing tissues. Oxidative stress is implicated in various neonatal conditions, including necrotizing enterocolitis, renal tubule damage, retinopathy of prematurity, and pain.