Background: Evidence is accumulating that mitochondrial (Mt) oxidative stress plays a role in the pathogenesis of preeclampsia. The current study analyzes the stress levels, energy status and associated enzymatic alteration in placental mitochondria of preeclamptic (ns30) and normotensive (ns35) subjects. Methods: Total Mt stress was measured using dichlorofluorescin (DCFH) oxidant analysis, malondialdehyde (MDA) concentrations, protein carbonyl (PC) concentrations and measurement of nitrite ( ) and

Preeclampsia is a disease of worldwide significance with increasing maternal mortality rate of 20-80 %. Though apoptosis is a normal constituent during pregnancy, there seems to be an altered balance between proliferation and apoptosis of endothelial cell in preeclampsia leading to a placental dysregulation resulting in premature delivery. Molecular chaperones like HSP70 and 90 play a significant role in control of preeclamptic progression and protect the developing fetus. This is governed by alterations in expression of HSF1, HIF1α a nuclear transcription factor and signaling molecule like ERK, JNK1/2, and Bcl-2. Endothelial cell from normotensive and preeclamptic placenta were analyzed for variation in viability and expression of signaling molecules. A significant decrease in viability of endothelial cell (p < 0.05) was noted in preeclamptic samples when compared to normotensive samples. The results indicate that there was an increase in, HSP70 and 90 (p < 0.01), HSF1 (p < 0.01), HIF1α (p < 0.05), ERK (p < 0.05), JNK1/2 (p < 0.05), and Bcl-2 (p < 0.05). Though there is a significant change in the viability of endothelial cell, the live fetal delivery is not predominantly affected during preeclampsia. The interplay between these signaling molecules which alter the apoptotic pathway to sustain endothelial cell viability is discussed.

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The over expression of HSP70 and HSF1 seen in the pre-eclamptic endothelial cells suggests its possible protective role as stress specific natural adaptive response against the generated stress.