Abstract

Objective: Oxidative stress occurs when cellular levels of reactive oxygen species exceed antioxidant capabilities and has been implicated in the pathogenesis of preeclampsia. Patients and Methods: In this study we measured the tissue levels of endogenous antioxidant proteins such as superoxide dismutase, glutathione peroxidase, glutathione reductase and in addition to the levels of homocysteine, lipid and protein oxidation in placental samples from normal and preeclamptic pregnancies. Results: Preeclamptic tissue homogenates demonstrated significantly increased levels of homocysteine 12.31 ± 2.10 versus 2.31 ± 3.22 μmole/l, increased levels of lipid peroxidation 23.77 ± 5.26 μM/ mg protein versus 6.22 ± 2.31 μM/ mg protein (p< 0.01) and a significance increase in protein carbonyl concentration 250.44 ± 48.23 versus 190.24 ± 26 .46 units/mg protein when compared to controls, while levels of the other antioxidant proteins, superoxide dismutase1.55 ± 0.22 versus4.42 ± 0.32 U/mg protein p<0.05, Glutathionereductase12.13+ 3.3 versus 22.24 ± 7.71 U/mg protein (P<0.05), Glutathione68.12 ± 14.22 versus 105 ± 16ng/mg protein (P<0.01) and glutathione peroxidase 10. 22 ± 5.33 versus15.22 ± 4.44 nmol/min /mg protein (P<0.05) were all found to be significantly reduced when comparing preeclamptic placental tissue homogenates to gestational age matched control placental from non preeclamptic pregnancies. Conclusions: The results of this study demonstrate placental oxidative stress through reduced antioxidant enzyme activities and hyperhomocystinemia which play a role in the pathogenesis of preeclampsia .These novel data further understanding the pathophysilology of preeclampsia and provides a new insight into the pathogenesis of clinical complications exhibited in this condition suggesting antioxidant therapy may be improving health of this condition.

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