Biomedical Research

The aetio-pathogenesis of preeclampsia, a complication of pregnancy, is poorly understood. Oxidative stress has been shown to be the causative factor for hyper-tension as well as for target tissue damage in hypertension. Studies that explain the role of oxidative stress in preeclampsia have been few in number. The present study was aimed at (1) determining the extent of oxidative stress in preeclampsia and measurement of lipid peroxidation as a marker of oxidative stress, (2) corre-lation of lipid peroxidation to ceruloplasmin levels and (3) correlation of lipid peroxidation to blood pressure changes and urinary protein excretion during the antenatal period as well as the post-partum period. Thirty women with preeclampsia, thirty normotensive pregnant women (who were matched for maternal and gestational age) and thirty normotensive, non-pregnant women were selected for the study. Lipid peroxidation was measured as malonaldehyde (MDA) levels, ceruloplasmin was quantitated by its oxidase ac-tivity and urinary protein excretion was determined by turbidometry. Lipid peroxidation was significantly increased in preeclampsia when compared to normotensive pregnant women. Malonaldehyde levels were moderately increased in normotensive pregnant controls (1.3nM/mL ± 0.15) and markedly increased in preeclamptic pregnant women (2.52nM/mL ± 0.22) when compared to non preg-nant normotensive women (0.91nM/mL ± 0.17). Oxidase activity of ceruloplas-min was significantly increased in preeclamptic women compared to normal pregnant women. A significant correlation was found between the increase in uric acid levels and ceruloplasmin in preeclamptic women. The elevated blood pres-sure returned to normal levels after delivery, but lipid peroxidation and urine protein excretion remained higher than normal, suggesting that factors other than oxidative stress may contribute to the development of hypertension in pree-clamptic women. Oxidative stress, however, plays a very important role in the causation of target tissue damage such as renal injury.

Author(s): Vanitha Gowda MN, Aroor AR, Krishna L
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