Preeclampsia (PE) characterized by hypertension and proteinuria developing after mid gestation- is the most severe form of hypertensive disorders in pregnancy. PE affects 2.7% of pregnancies and represents a major cause of maternal and prenatal morbidity and mortality. The pathogenetic mechanism of PE are still debated. Current hypotheses include immune maladaptaion, placental ischemia, inflammation, dyslipidemia and genetic predisposition. Increasing evidence suggests that placental and systemic oxidative stress place a crucial role in the development of PE. PE is a two-stage disorder. Stage one PE is poor placentation, which is followed by the development of maternal syndrome. Poor placentation with subsequent uteroplacental insufficiency leads to placental ischemia and oxidative stress. The ischemic and oxidatively stressed placenta releases proinflammatory (Th1) cytokines, lipid peroxidation products and trophoblast debris into the maternal circulation which in turn trigger a systemic inflammatory response. The systemic inflammatory response with systemic oxidative stress appears to be the cause of the maternal syndrome of preeclampsia.