In this proposal we test the role of oxidative stress in the pathophysiology of preeclampsia. Oxidative stress generates free radicals that injure tissues, especially vascular endothelial cell function as components of oxidized LDL (ox-LDL), alter endothelial cell structure and function. Data from our lab and others support alterations of endothelial cell function as a component of the pathophysiology of preeclampsia. In addition, preliminary data from our group indicates potential generation of pro oxidants by preeclamptic placenta. We demonstrated increased xanthine oxidase/dehydrogenase, an enzyme which can generate superoxide, in invasive cytotrophoblast from preeclamptic women. We recently demonstrated material in the blood or plasma of preeclamptic women that increases ascorbate oxidation in vitro. We propose to characterize the activity. Whether these findings indicate cause or effect or are an epiphenomenon cannot be answered by available data. We propose definitively testing a causal role. We will study circulating markers of oxidative stress before, during and after preeclampsia.
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