Preeclampsia is a multisystemic disorder of pregnancy that causes perinatal morbidity and mortality. Studies published in the last decade have contributed to a better understanding of physiopathogenesis through key mechanisms involved, such as altered immune response, endothelial dysfunction, oxidative stress and systemic inflammatory response, as well as genetic susceptibility. Oxidative stress (OS) plays an important role in the development of preeclampsia, since it alters placental remodeling and placental vascular endothelial dysfunction, resulting in an ischemia/reperfusion injury with an increase in xanthine oxidase activity that produces high levels of reactive oxygen species (ROS). ROS can be generated through many pathways within cells, mitochondria, endoplasmic reticulum (ER) and enzymes such as NADPH oxidase are the most important sources, causing widespread and indiscriminate damage to cells and tissues, which leads to an intravascular inflammatory response and maternal systemic endothelial dysfunction characteristic of this prenatal syndrome. Therefore, the following review aims to identify the main risk factors and the role of OS as a pathophysiological mechanism in the development of preeclampsia.

中文翻译：

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妊娠期并发先兆子痫的氧化应激。

子痫前症是一种多系统性妊娠疾病，会引起围产期发病和死亡。过去十年中发表的研究通过涉及的关键机制，例如改变的免疫反应，内皮功能障碍，氧化应激和全身性炎症反应以及遗传易感性，帮助人们更好地理解了生理病理学。氧化应激（OS）在先兆子痫的发展中起重要作用，因为它改变胎盘重塑和胎盘血管内皮功能障碍，导致缺血/再灌注损伤，黄嘌呤氧化酶活性增加，产生高水平的活性氧（ROS） ）。ROS可以通过细胞，线粒体，内质网（ER）和酶（例如NADPH氧化酶）是最重要的来源，会对细胞和组织造成广泛且不加区分的损害，从而导致血管内炎症反应和这种产前综合症的母体全身内皮功能障碍。因此，以下综述旨在确定先兆子痫发展过程中的主要危险因素以及OS作为病理生理机制的作用。