Gupta Sajal, Agarwal Ashok, Sharma Rakesh K
Center for Advanced Research in Human Reproduction, Infertility, and Sexual Function, Glickman Urological Institute and the Department of Obstetrics-Gynecology, The Cleveland Clinic Foundation, Cleveland, Ohio 44195, USA.
Obstet Gynecol Surv. 2005 Dec;60(12):807-16. doi: 10.1097/01.ogx.0000193879.79268.59.
Preeclampsia is a complex multisystem disorder exclusively seen in human species that is characterized by hypertension and proteinuria. This disorder has the highest maternal and fetal morbidity and mortality of all pregnancy-related complications. Growing evidence suggests that placental oxidative stress is involved in the etiopathogenesis of preeclampsia. Reduced perfusion as a result of abnormal placentation leads to ischemia reperfusion injury to the placenta. Placental oxidative stress, which results from the ischemia reperfusion injury, is being increasingly reported to be involved in the etiopathogenesis of preeclampsia. It has been proposed as a promoter of lipid peroxidation and the endothelial cell dysfunction that is commonly seen in this condition. Although preeclampsia is characterized by increased lipid peroxidation and diminished antioxidant capacity, there is no consensus regarding causality of lipid peroxidation in preeclampsia. In this article, we address the question of the biologic association of lipid peroxidation and preeclampsia. Lipid peroxidation and leukocyte activation may play a pivotal role in endothelial cell dysfunction. We also review the different factors that have been proposed to cause endothelial cell dysfunction in preeclampsia, trials investigating the role of antioxidant supplementation in preeclampsia, and the lack of consensus among the trials. Additional longitudinal studies are necessary to determine if the various oxidative stress biomarkers estimated early in pregnancy can be narrowed to a single marker for predicting preeclampsia.
Obstetricians & Gynecologists, Family Physicians.
After completion of this article, the reader should be able to recall that placental oxidative stress is involved in the etiopathogenesis of preeclampsia, state that placental oxidative stress results from ischemic reperfusion injury, and explain that ischemic reperfusion injury is a promoter of lipid peroxidation and endothelial cell dysfunction seen in preeclampsia.
子痫前期是一种仅在人类中出现的复杂多系统疾病，其特征为高血压和蛋白尿。该疾病在所有与妊娠相关的并发症中，孕产妇和胎儿的发病率及死亡率最高。越来越多的证据表明，胎盘氧化应激参与了子痫前期的发病机制。胎盘形成异常导致的灌注减少会引起胎盘的缺血再灌注损伤。越来越多的报道称，由缺血再灌注损伤引起的胎盘氧化应激参与了子痫前期的发病机制。它被认为是子痫前期常见的脂质过氧化和内皮细胞功能障碍的促进因素。尽管子痫前期的特征是脂质过氧化增加和抗氧化能力下降，但关于脂质过氧化在子痫前期中的因果关系尚无共识。在本文中，我们探讨脂质过氧化与子痫前期的生物学关联问题。脂质过氧化和白细胞激活可能在内皮细胞功能障碍中起关键作用。我们还回顾了已提出的导致子痫前期内皮细胞功能障碍的不同因素、研究抗氧化剂补充在子痫前期中作用的试验，以及这些试验之间缺乏共识的情况。需要更多的纵向研究来确定妊娠早期估计的各种氧化应激生物标志物是否可以缩小为预测子痫前期的单一标志物。
妇产科医生、家庭医生。
阅读本文后，读者应能够回忆起胎盘氧化应激参与子痫前期的发病机制，指出胎盘氧化应激由缺血再灌注损伤引起，并解释缺血再灌注损伤是子痫前期中脂质过氧化和内皮细胞功能障碍的促进因素。
