Abstract

Data on respiratory burst activity of granulocytes from healthy and preeclamptic pregnant women are contradictory. To further investigate a possible role of reactive oxygen species in the etiology of preeclampsia, the induced superoxide-anion generation by granulocytes from non-pregnant, healthy pregnant and preeclamptic pregnant women were measured. The reciprocal effects of heat-inactivated and non-inactivated plasma on superoxide production by neutrophils from non-pregnant, healthy pregnant and preeclamptic pregnant subjects were also examined. Superoxide generation was measured by ferricytochrome c reduction. Both phorbol-12.13-dibutirate- and N-formyl-methionyl-leucyl-phenylalanine-induced superoxide production was significantly decreased in normal pregnancy compared to results obtained in non-pregnant and preeclamptic pregnant women. Phorbol-12.13-dibutirate-induced superoxide generation by non-pregnant and preeclamptic neutrophils was significantly inhibited by heat-inactivated and non-inactivated healthy pregnant plasma. N-formyl-methionyl-leucyl-phenylalanine-stimulated superoxide production by non-pregnant and preeclamptic granulocytes was suppressed only by non-inactivated healthy pregnant plasma. Phorbol-12.13-dibutirate-induced superoxide generation of healthy pregnant neutrophils was significantly increased by inactivated and non-inactivated non-pregnant and preeclamptic plasma. N-formyl-methionyl-leucyl-phenylalanine-stimulated superoxide production by healthy pregnant granulocytes was significantly enhanced following treatment of the cells with non-inactivated non-pregnant and preeclamptic pregnant plasma. Deficient superoxide generation in normal pregnancy may be caused by maternal immunosuppressive factors. The failure of reduction in superoxide production in preeclampsia may be partly responsible for endothelial dysfunction. Apart from oxidative stress, a possible role of inefficient maternal immunosuppression should also be considered in the pathogenesis of preeclampsia.

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