Department of Clinical and Experimental Medicine and Pharmacology, School of Medicine, University of Messina, Via C. Valeria - Gazzi - 98100 Messina, Italy.
Curr Pharm Des. 2012;18(26):3889-900. doi: 10.2174/138161212802083716.
Reactive oxygen species (ROS) are well recognized for playing a dual role as both deleterious and beneficial species. ROS are products of normal cellular metabolism and under physiological conditions, participate in maintenance of cellular 'redox homeostasis. Overproduction of ROS, results in oxidative stress. Oxidative stress is a deleterious process that leads to lung damage and consequently to various disease states. The lung is a highly specialized organ that facilitates uptake of oxygen and release of carbon dioxide. Persistent inhalation of the invading pathogens or toxic agents may result in overwhelming production of ROS. Oxidants initiate a number of pathologic processes, including inflammation of the airways, which may contribute to the pathogenesis and/or exacerbation of airways disease. During inflammation, enhanced ROS production may induce recurring DNA damage, inhibition of apoptosis, and activation of protooncogenes by initiating signal transduction pathways. Therefore, it is conceivable that chronic inflammation-induced production of ROS in the lung may predispose individuals to lung diseases. In this review, we discuss mechanisms of oxidant stress in the lung, the role of oxidants in lung disease pathogenesis and exacerbation.
活性氧（ROS）被认为在有害和有益物种中都具有双重作用。ROS 是正常细胞代谢的产物，在生理条件下，参与维持细胞的“氧化还原平衡”。ROS 的过度产生会导致氧化应激。氧化应激是一种有害过程，会导致肺部损伤，进而导致各种疾病状态。肺是一种高度特化的器官，可促进氧气的摄取和二氧化碳的释放。持续吸入入侵的病原体或有毒物质可能会导致 ROS 的过度产生。氧化剂会引发多种病理过程，包括气道炎症，这可能有助于气道疾病的发病机制和/或恶化。在炎症过程中，ROS 产生的增强可能会通过启动信号转导途径导致反复的 DNA 损伤、细胞凋亡抑制和原癌基因的激活。因此，可以想象，肺部慢性炎症引起的 ROS 产生可能使个体易患肺部疾病。在这篇综述中，我们讨论了肺部氧化应激的机制，以及氧化剂在肺部疾病发病机制和恶化中的作用。
