ROLE OF MALONDIALDEHYDE IN THE PATHOGENESIS OF PREECLAMSIA

Abstract

Background: The exact cause of preeclampsia is unclear but one of the hypotheses in this regard is that preeclampsia caused by vascular endothelial dysfunction due to increase in circulating free radicals such as lipid peroxides which are determined by malondialdehyde.Objective: To evaluate the possible involvement of lipid peroxidation in form of malondialdehyde (MDA) in the pathogenesis of pre-eclampsia.Methods: The present study conducted on a total of 100 Kurdish women in their 3rd trimester of pregnancy admitted to the Gynecologic and Obstetric hospital in Sulaymania city at period of February to June 2007. Maternal blood was collected for determination of basal and post delivery MDA levels of the studied preeclamptic patients and normotensive pregnant controls. In addition, cord blood was collected immediately after delivery from a 25 preeclamptic patients and a 25 normotensive pregnant women delivered by cesarean section.Results: Statistical analysis reveals that there is significantly higher levels of MDA both in maternal and cord blood of preeclamptic patients compared to normotensive pregnant control (P<0.0025, P<0.015) respectively.Furthermore, a significant positive correlation between maternal serum and cord blood MDA was found in preeclamptic pregnancies (r=0.59, P<0.0005). A significant increment of basal serum MDA level was demonstrated in normotensive pregnant women delivered by normal vaginal delivery (NVD) (P<0.018). On the other hand, no statistical significantchanges were observed in serum MDA level of normotensive women delivered by cesarean section (P>0.77). Serum MDA in preeclamptic patients rose significantly above the preoperative value within one day postoperatively (1.48±0.55; P<0.01) then tend to fall significantly (0.9±0.46; P<0.02) toward the normal basal level (0.89±0.6) after two days post operatively.Conclusions: High levels of MDA in the serum of preeclamptic patients and their placenta may play a role in the pathogenesis of preeclampsia.