Isoprostanes and asthma.
Isoprostanes and asthma.
复制标题
异前列烷和哮喘。
DOI：
10.1016/j.bbagen.2011.04.016
复制
发表时间：
2011
期刊：
影响因子：
--
通讯作者：
Kummarapurugu,Apparao
中科院分区：
文献类型：
--
作者：
Voynow,JudithA;Kummarapurugu,Apparao
异前列腺素是体内多不饱和脂肪酸（包括花生四烯酸）在氧化应激后产生的前列腺素（PG）样化合物。它们是根据它们的前列腺环结构和碳侧链上羟基的定位来命名的；这些结构上的差异导致了具有不同生物学特性的异前列腺素分子的广泛分布。特异性异前列腺素的产生也受宿主细胞氧化还原条件的调节；还原条件有利于f2 -异前列腺素的生成，而在缺乏抗氧化能力的条件下，形成D2-和e2 -异前列腺素。f2 -异前列腺素（F2-isoP）被认为是包括哮喘在内的肺部疾病中氧化应激的可靠标志物。重要的是，F2-isoP和其他异前列腺素作为PG受体的配体，以及潜在的其他尚未确定的受体。据报道，它们在许多器官中具有重要的生物学特性。在肺中，异前列腺素调节影响气道平滑肌张力、神经分泌、上皮离子通量、内皮细胞粘附和通透性以及巨噬细胞粘附和功能的细胞过程。在这篇综述中，我们将总结F2-isoP作为哮喘氧化应激标志物的证据，以及F2-isoP和其他异前列腺素在哮喘发病机制中发挥生物学作用的证据。这篇文章是《哮喘生物化学》特刊的一部分。
Isoprostanes are prostaglandin (PG)-like compounds generated in vivo following oxidative stress by non-enzymatic peroxidation of polyunsaturated fatty acids, including arachidonic acid. They are named based on their prostane ring structure and by the localization of hydroxyl groups on the carbon side chain; these structural differences result in a broad array of isoprostane molecules with varying biological properties. Generation of specific isoprostanes is also regulated by host cell redox conditions; reducing conditions favor F2-isoprostane production while under conditions with deficient antioxidant capacity, D2- and E2-isoprostanes are formed. F2-isoprostanes (F2-isoP) are considered reliable markers of oxidative stress in pulmonary diseases including asthma. Importantly, F2-isoP and other isoprostanes function as ligands for PG receptors, and potentially other receptors that have not yet been identified. They have been reported to have important biological properties in many organs. In the lung, isoprostanes regulate cellular processes affecting airway smooth muscle tone, neural secretion, epithelial ion flux, endothelial cell adhesion and permeability, and macrophage adhesion and function. In this review, we will summarize the evidence that F2-isoP functions as a marker of oxidative stress in asthma, and that F2-isoP and other isoprostanes exert biological effects that contribute to the pathogenesis of asthma. This article is part of a Special Issue entitled Biochemistry of Asthma.