Abstract：
Oxidative stress results from the production of reactive oxygen species (ROS) and reactive nitrogen species (RNS) in quantities exceeding the potential activity of the body\'s antioxidant system and is one of the risk factors for the development of vascular dysfunction in diabetes and exposure to ionizing radiation. Being the secondary products of normal aerobic metabolism in living organisms, ROS and RNS act as signaling molecules that play an important role in the regulation of vital organism functions. Meanwhile, in high concentrations, these compounds are toxic and disrupt various metabolic pathways. The various stress factors (hyperglycemia, gamma-irradiation, etc.) trigger free oxygen and nitrogen radicals accumulation in cells that are capable to damage almost all cellular components including ion channels and transporters such as Na+/K+-ATPase, BKCa, and TRP channels. Vascular dysfunctions are governed by interaction of ROS and RNS. For example, the reaction of ROS with NO produces peroxynitrite (ONOO-), which not only oxidizes DNA, cellular proteins, and lipids, but also disrupts important signaling pathways that regulate the cation channel functions in the vascular endothelium. Further increasing in ROS levels and formation of ONOO- leads to reduced NO bioavailability and causes endothelial dysfunction. Thus, imbalance of ROS and RNS and their affect on membrane ion channels plays an important role in the pathogenesis of vascular dysfunction associated with various disorders.
摘要：
氧化应激是由活性氧（ROS）和活性氮（RNS）产生的，其数量超过人体抗氧化系统的潜在活性，是糖尿病和暴露于电离辐射中血管功能障碍发展的危险因素之一。作为生物体正常有氧代谢的次级产物，ROS和RNS充当信号分子，在调节重要的生物体功能中起重要作用。同时,在高浓度下，这些化合物是有毒的，破坏各种代谢途径。各种应激因素(高血糖，γ-辐照,等。）触发细胞中的游离氧和氮自由基积累，这些自由基能够破坏几乎所有细胞成分，包括离子通道和转运蛋白，例如Na/K-ATPase，BKCa,和TRP频道。血管功能障碍由ROS和RNS的相互作用控制。例如,ROS与NO的反应产生过氧亚硝酸盐（ONOO-），不仅氧化DNA，细胞蛋白质，和脂质，但也破坏了调节血管内皮阳离子通道功能的重要信号通路。ROS水平的进一步增加和ONOO-的形成导致NO生物利用度降低并引起内皮功能障碍。因此，ROS和RNS的失衡及其对膜离子通道的影响在与各种疾病相关的血管功能障碍的发病机制中起着重要作用。
