Pathogenesis of preeclampsia: Implications of apoptotic markers and oxidative stress.

This study aimed to investigate the implication of some apoptotic and lipid peroxidation markers in preeclampsia (PE). A total of 25 women with PE and 25 age- and parity-matched normal pregnant women were enrolled in this study. The malondialdehyde (MDA) level, caspase-9 activity and the percentage of DNA fragmentation were significantly higher in placental tissue of PE than in control women. The serum level of MDA was significantly elevated in women with PE having delivery by cesarean section (CS) than in women with PE having vaginal delivery. In vitro study demonstrated that the addition of 0.5 mM Fe(2+) and 0.1 mM ascorbate caused increase in the production of MDA level in placental tissue with PE than normal placentas, and vitamin E (100 µM) caused lower inhibition of in vitro lipid peroxidation in placental tissue with PE when compared with normal tissue. The activity of caspase-9 and percentage of DNA fragmentation were associated with the severity of the PE and both could differentiate between PE and control women with 88% and 100% sensitivity and 96% and 100% specificity, respectively. The activities of caspase-8 and/or -9 were positively correlated with the maternal age but only caspase-8 was negatively correlated with neonatal birth weight and placental weight. In conclusion, the elevations of MDA, caspase-9 activity and the percentage of DNA fragmentation in the placentas of women with PE implicate the involvement of lipid peroxidation and apoptosis in PE. The placenta represents a considerable source of the elevated circulating MDA in PE.