Lung oxidative damage by hypoxia.
Lung oxidative damage by hypoxia.
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DOI：
10.1155/2012/856918
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发表时间：
2012
影响因子：
--
通讯作者：
Tuesta M
中科院分区：
文献类型：
--
作者：
Araneda OF;Tuesta M
肺最重要的功能之一是维持机体内足够的氧合。这个器官可以受到缺氧的影响，面临生理和病理情况。暴露于这种情况有利于增加来自线粒体的活性氧，如来自NADPH氧化酶、黄嘌呤氧化酶/还原酶和一氧化氮合酶，以及建立炎症过程。在肺中，缺氧也改变了抗氧化物质的水平，导致肺氧化损伤。缺氧诱导的肺氧化还原状态的不平衡已被认为是在缺氧背景下观察到的肺功能变化的参与者，如缺氧性血管收缩和肺水肿，以及血管重塑和慢性肺动脉高压。在这项工作中，实验证据表明，在肺缺氧氧化还原状态的隐含机制进行了审查。在此，描述了不同肺细胞和完全分离的肺的培养物的研究以及在不同形式的缺氧中在动物模型和人中进行的体内进行的测试。
One of the most important functions of lungs is to maintain an adequate oxygenation in the organism. This organ can be affected by hypoxia facing both physiological and pathological situations. Exposure to this condition favors the increase of reactive oxygen species from mitochondria, as from NADPH oxidase, xanthine oxidase/reductase, and nitric oxide synthase enzymes, as well as establishing an inflammatory process. In lungs, hypoxia also modifies the levels of antioxidant substances causing pulmonary oxidative damage. Imbalance of redox state in lungs induced by hypoxia has been suggested as a participant in the changes observed in lung function in the hypoxic context, such as hypoxic vasoconstriction and pulmonary edema, in addition to vascular remodeling and chronic pulmonary hypertension. In this work, experimental evidence that shows the implied mechanisms in pulmonary redox state by hypoxia is reviewed. Herein, studies of cultures of different lung cells and complete isolated lung and tests conducted in vivo in the different forms of hypoxia, conducted in both animal models and humans, are described.
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