人肺炎症状态下氧代谢产物的产生和降解。

Vuokko L Kinnula
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引用次数: 56

摘要

肺是一个遭受高氧化负担的组织,但也被赋予了有效的保护,防止氧气和活性氧(ROS)。肺部所经历的氧化应激会因外源性氧化剂产生毒素(最重要的是污染物和香烟烟雾)以及肺部炎症期间氧化剂产生的增加而增强。人肺中存在的主要氧化酶包括NADPH氧化酶、髓过氧化物酶、嗜酸性粒细胞过氧化物酶和一氧化氮合酶,它们都是在炎症状态下诱导产生的。人体肺部对抗活性氧的抗氧化机制比通常认为的更通用。除了金属结合蛋白、黏液成分、小分子量抗氧化剂和维生素外,肺组织还具有高度细胞特异性和区隔化的防御系统,该系统包含几种位置、诱导性和动力学各异的抗氧化酶。哮喘、慢性阻塞性肺疾病(COPD)和肺实质疾病等炎症状态已被证明会导致肺部氧化/抗氧化平衡的严重紊乱,从而导致氧化介导的细胞损伤。新型合成抗氧化剂模拟物可能具有减缓或终止与自由基相关的肺部疾病进展的潜力。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Production and degradation of oxygen metabolites during inflammatory states in the human lung.

Lung represents a tissue that encounters a high oxidant burden but is also endowed with efficient protection against oxygen and reactive oxygen species (ROS). The oxidant stress experienced by the lung is enhanced by exogenous oxidant producing toxins most importantly pollutants and cigarette smoke, as well as by increased oxidant production during lung inflammation. The major oxidant generating enzymes present in human lung include NADPH oxidase, myeloperoxidase, eosinophil peroxidase and nitric oxide synthases, all of which are induced during inflammatory states. The antioxidant machinery of human lung against ROS is more versatile than often assumed. In addition to metal binding proteins, mucus components and small molecular weight antioxidants and vitamins, lung tissue possesses a highly cell specific and compartmentalized defense system containing several antioxidant enzymes with variable locations, inducibilities and kinetics. Inflammatory states like asthma, chronic obstructive lung disease (COPD) and parenchymal lung disorders have been shown to lead to serious disturbances in the oxidant/antioxidant balance of the lung with consequent oxidant mediated cell injury. Novel synthetic antioxidant mimetics may have the potential to slow or terminate the progression of lung diseases associated with free radicals.

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