Bilodeau Jean-François, Hubel Carl A
Department of Obstetrics and Gynecology, Laval University and CHUL Research Centre, Québec, QC, Canada.
J Obstet Gynaecol Can. 2003 Sep;25(9):742-50. doi: 10.1016/s1701-2163(16)31003-9.
Preeclampsia is a leading cause of maternal and neonatal mortality and morbidity. It is a complex syndrome of undetermined etiologic origin, usually diagnosed during the second half of pregnancy, with clinical features of hypertension, proteinuria, and edema. No cure for preeclampsia exists, except premature delivery. There is increasing evidence that oxidative stress is an important contributing factor to the pathogenesis of preeclampsia. Oxidative stress is defined as an imbalance between reactive oxygen species (ROS), such as nitric oxide (NO*), superoxide anion (O2*-), and hydrogen peroxide (H2O2), and antioxidants, favouring an overabundance of ROS. The consequence of an overproduction of ROS can be observed as increased levels of markers of oxidative stress, such as lipid peroxides. Pregnant women affected by preeclampsia may have abnormal ROS production, particularly NO* and O2*-, abnormal levels of antioxidant defences, and increased placental lipid peroxidation. Several observations suggest that decreased bioavailability of endothelium-derived NO*, due to oxidative destruction of NO* by ROS, might contribute to the impaired endothelium-dependent vasodilatory responses and multisystemic pathology of preeclampsia, a phenomenon in which antioxidant vitamins may play a beneficial role. This review focuses on the rationale for vitamins C and E supplementation toward prevention of preeclampsia, with an emphasis on the limit of our scientific knowledge concerning the deleterious oxidative events taking place in this pathology.
子痫前期是孕产妇和新生儿发病及死亡的主要原因。它是一种病因不明的复杂综合征，通常在妊娠后半期被诊断出来，具有高血压、蛋白尿和水肿等临床特征。除了早产外，尚无治愈子痫前期的方法。越来越多的证据表明，氧化应激是子痫前期发病机制的一个重要促成因素。氧化应激被定义为活性氧（ROS）如一氧化氮（NO*）、超氧阴离子（O2*-）和过氧化氢（H2O2）与抗氧化剂之间的失衡，导致ROS过量。ROS产生过多的后果可表现为氧化应激标志物水平升高，如脂质过氧化物。受子痫前期影响的孕妇可能存在ROS产生异常，尤其是NO和O2-，抗氧化防御水平异常，以及胎盘脂质过氧化增加。多项观察表明，由于ROS对NO的氧化破坏导致内皮源性NO的生物利用度降低，可能导致子痫前期内皮依赖性血管舒张反应受损和多系统病变，而抗氧化维生素可能在这一现象中发挥有益作用。本综述重点关注补充维生素C和E预防子痫前期的理论依据，同时强调我们对该病理过程中有害氧化事件的科学认识的局限性。
