Abstract
Preeclampsia (PE) is characterized by disturbed extravillous trophoblast migration toward uterine spiral arteries leading to increased uteroplacental vascular resistance and by vascular dysfunction resulting in reduced systemic vasodilatory properties. Its pathogenesis is mediated by an altered bioavailability of nitric oxide (NO) and tissue damage caused by increased levels of reactive oxygen species (ROS). Furthermore, superoxide (O2−) rapidly inactivates NO and forms peroxynitrite (ONOO−). It is known that ONOO− accumulates in the placental tissues and injures the placental function in PE. In addition, ROS could stimulate platelet adhesion and aggregation leading to intravascular coagulopathy. ROS-induced coagulopathy causes placental infarction and impairs the uteroplacental blood flow in PE. The disorders could lead to the reduction of oxygen and nutrients required for normal fetal development resulting in fetal growth restriction. On the other hand, several antioxidants scavenge ROS and protect tissues against oxidative damage. Placental antioxidants including catalase, superoxide dismutase (SOD), and glutathione peroxidase (GPx) protect the vasculature from ROS and maintain the vascular function. However, placental ischemia in PE decreases the antioxidant activity resulting in further elevated oxidative stress, which leads to the appearance of the pathological conditions of PE including hypertension and proteinuria. Oxidative stress is defined as an imbalance between ROS and antioxidant activity. This review provides new insights about roles of oxidative stress in the pathophysiology of PE.
Highlights
Preeclampsia (PE) is a pregnancy-induced hypertensive disorder associated with proteinuria that occurs after the 20th gestational week
We demonstrated that sera derived from patients with PE stimulated the expression of gp91phox of vascular nicotinamide adenine dinucleotide phosphate (NADPH) oxidase via tumor necrosis factor α (TNFα) and angiotensin II receptor subtype 1 (AT1) [23,26]
superoxide dismutase (SOD) is increased during normal pregnancy [77], and, SOD activity and mRNA expression of CuZn-SOD in the placental tissue derived from patients with PE is decreased, which may result in increased oxidative stress in the placenta of patients with PE [85]
Summary
Preeclampsia (PE) is a pregnancy-induced hypertensive disorder associated with proteinuria that occurs after the 20th gestational week. Vascular dysfunction of the placenta results in placental secretion of humoral factors into the maternal systemic circulation. These humoral factors trigger multiple organ injuries responsible for the clinical manifestations of PE. Hypoxic placenta induces the production and secretion of humoral factors into maternal systemic circulation. These factors disturb vascular endothelial function resulting in multiple organ failure at the second step. ONOO− formation are known to reduce the bioavailability of NO and cause endothelial dysfunction These effects could be key elements in the pathogenesis of PE. Activated neutrophils produce ROS through the action of several activated enzymes, including NADPH oxidase [19,20], xanthine oxidase (XO), and uncoupled eNOS [21]
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