Dyslipidemia, iron, and oxidative stress in preeclampsia: assessment of maternal and feto-placental interactions.

Abstract

The etiology and pathogenesis of the pregnancy syndrome preeclampsia remain poorly understood. There is evidence that oxidative stress (am imbalance between oxidant and antioxidant forces in favor of oxidants) occurs in preeclampsia, and it has been hypothesized that reactive oxygen species or their metabolites ultimately comprise the "defensive" vasodilatory, antiaggregatory, and barrier functioning of the vascular endothelium. Oxidative stress may be point at which feto-placental and maternal factors converge, resulting in the protean manifestations of preeclampsia. This review highlights the evidence for maternal dyslipidemia and altered iron kinetics in preeclampsia and gives a critical assessment of their potential impact on disease progression. The theme is developed that interaction of maternal components, particularly neutrophils and oxidation-susceptible lipids, with placental cells and placental-derived factors engenders feed-forward cycles of oxidative stress that ultimately cause widespread endothelial cell dysfunction and its clinical manifestations.