Plasma nitric oxide, endothelin-1, arginase and superoxide dismutase in the plasma and placentae from preeclamptic patients.

The aim of this study was to determine parameters of NO metabolism in plasma and placenta of preeclamptic (PE) patients. It was conducted a case-control study at São José Hospital, Brazil. Thirty-three PE and 33 normotensive pregnant were included in the study. The diagnosis of PE was established in accordance with the definitions of American College of Obstetricians and Gynecologists. Peripheral venous blood and placenta samples were obtained at postpartum period. Plasma NO levels and SOD activity were significantly lower and endothelin-1 levels and arginase activity were significantly higher in PE women when compared to controls. None of the analyzed parameters were different in the placenta between groups. Our findings suggest that parameters associated with NO metabolism are altered only at the systemic level, but not in placenta of PE patients.

Oxidative damage, inflammation, and Toll-like receptor 4 pathway are increased in preeclamptic patients: a case-control study.

PROBLEM: There was no direct correlation between plasma and placental oxidative damage parameters and inflammation and evidence of TLR4 pathway activation in the placenta in preeclamptic (PE) patients. METHOD OF STUDY: 33 PE patients and 33 normotensive pregnant women were included. The maternal section of the placenta and blood were collected to the determination of oxidative damage markers (thiobarbituric acid reactive species and protein carbonyls), inflammatory response (interleukin-6 and myeloperoxidase activity), and activation of the TLR-4-NF-kB pathway. RESULTS: An increase of IL-6 levels in both plasma and placenta was observed, but myeloperoxidase activity was not significantly different comparing the groups. Oxidative damage parameters were increased in plasma and placenta in PE patients. A significant increase of the protein levels of TLR-4 and NF-kB was observed in the placenta. CONCLUSION: The TLR4-NF-kB pathway is upregulated in PE, probably generating local and systemic inflammatory response that is followed by local and systemic oxidative damage.