Abstract
The etiology and pathogenesis of the pregnancy syndrome preeclampsia remain poorly
understood. There is evidence that oxidative stress (an 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 compromise
the “defensive” vasodilatory, antiaggregatory, and barrier functioning of the vascular
endothelium. Oxidative stress may be a 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.
Keywords:
Preeclampsia - maternal dyslipidemia - iron kinetics - oxidative stress
