Department of Obstetrics and Gynecology, Medical and Health Science Center, University of Debrecen, Nagyerdei krt. 98, Debrecen 4012, Hungary.
J Reprod Immunol. 2011 May;89(2):199-206. doi: 10.1016/j.jri.2011.01.019. Epub 2011 May 6.
Data on the respiratory burst activity of granulocytes from healthy and preeclamptic women have remained contradictory. To investigate the role of reactive oxygen species in the etiology of preeclampsia we measured superoxide anion generation by granulocytes from non-pregnant, healthy, and preeclamptic women. We also examined the reciprocal effects of heat-inactivated and non-inactivated plasma on superoxide production. Superoxide generation was measured by ferricytochrome-c reduction. Superoxide production induced by either phorbol-12,13-dibutirate or N-formyl-methionyl-leucyl-phenylalanine was significantly decreased in granulocytes from normal pregnant women compared with non-pregnant and preeclamptic women. The phorbol-12,13-dibutirate-induced superoxide generation by granulocytes from non-pregnant and preeclamptic women was significantly inhibited by plasma from healthy pregnant women. The N-formyl-methionyl-leucyl-phenylalanine-stimulated superoxide production by granulocytes from non-pregnant and preeclamptic women was suppressed only by non-inactivated plasma, not heat-inactivated plasma from healthy pregnant women. Plasma from preeclamptic women did not influence the phorbol-12,13-dibutirate- and N-formyl-methionyl-leucyl-phenylalanine-induced superoxide production by control granulocytes. The phorbol-12,13-dibutirate-induced superoxide generation by granulocytes from healthy pregnant women was significantly increased by the effect of plasma from non-pregnant and preeclamptic women, but when stimulating with N-formyl-methionyl-leucyl-phenylalanine only non-inactivated plasma caused the same enhancement. These data indicate that reduced superoxide generation in normal pregnancy may be caused by maternal immunosuppressive factors present in plasma. The failure to reduce superoxide production in preeclampsia may be partly responsible for the endothelial dysfunction characteristic of that condition.
关于健康孕妇和子痫前期孕妇的粒细胞呼吸爆发活性的数据一直存在争议。为了研究活性氧在子痫前期发病机制中的作用，我们测量了非妊娠、健康和子痫前期孕妇的粒细胞产生超氧阴离子。我们还研究了热失活和未失活血浆对超氧化物产生的相互影响。通过铁细胞色素 c 还原法测量超氧化物的产生。与非妊娠和子痫前期妇女相比，正常妊娠妇女的粒细胞产生的佛波醇 12,13-二丁酸酯或 N-甲酰基-甲硫氨酸-亮氨酸-苯丙氨酸诱导的超氧化物生成明显减少。来自非妊娠和子痫前期妇女的粒细胞的佛波醇 12,13-二丁酸酯诱导的超氧化物生成被来自健康妊娠妇女的血浆显著抑制。仅未失活的血浆而非来自健康妊娠妇女的热失活血浆抑制了 N-甲酰基-甲硫氨酸-亮氨酸-苯丙氨酸刺激的非妊娠和子痫前期妇女的粒细胞产生的超氧化物。来自子痫前期妇女的血浆不影响对照粒细胞中佛波醇 12,13-二丁酸酯和 N-甲酰基-甲硫氨酸-亮氨酸-苯丙氨酸诱导的超氧化物产生。来自健康妊娠妇女的粒细胞的佛波醇 12,13-二丁酸酯诱导的超氧化物生成通过来自非妊娠和子痫前期妇女的血浆的作用显著增加，但当用 N-甲酰基-甲硫氨酸-亮氨酸-苯丙氨酸刺激时，只有未失活的血浆引起相同的增强。这些数据表明，正常妊娠中超氧化物生成减少可能是由于血浆中存在的母体免疫抑制因子引起的。子痫前期中超氧化物产生减少的失败可能是该疾病特征性内皮功能障碍的部分原因。
