Department of Thoracic Medicine and Surgery, Temple University, Philadelphia, PA 19140, USA.
Center for Inflammation, Translational and Clinical Lung Research, Temple University, Philadelphia, PA 19140, USA.
Oxid Med Cell Longev. 2018 Feb 11;2018:5730395. doi: 10.1155/2018/5730395. eCollection 2018.
Chronic obstructive pulmonary disease (COPD) includes chronic bronchitis and emphysema. Environmental exposure, primarily cigarette smoking, can cause high oxidative stress and is the main factor of COPD development. Cigarette smoke also contributes to the imbalance of oxidant/antioxidant due to exogenous reactive oxygen species (ROS). Moreover, endogenously released ROS during the inflammatory process and mitochondrial dysfunction may contribute to this disease progression. ROS and reactive nitrogen species (RNS) can oxidize different biomolecules such as DNA, proteins, and lipids leading to epithelial cell injury and death. Various detoxifying enzymes and antioxidant defense systems can be involved in ROS removal. In this review, we summarize the main findings regarding the biological role of ROS, which may contribute to COPD development, and cytoprotective mechanisms against this disease progression.
慢性阻塞性肺疾病（COPD）包括慢性支气管炎和肺气肿。环境暴露，主要是吸烟，会导致高水平的氧化应激，是 COPD 发展的主要因素。香烟烟雾还会由于外源性活性氧（ROS）导致氧化还原失衡。此外，在炎症过程中和线粒体功能障碍期间内源性释放的 ROS 也可能导致疾病进展。ROS 和活性氮物种（RNS）可以氧化不同的生物分子，如 DNA、蛋白质和脂质，导致上皮细胞损伤和死亡。各种解毒酶和抗氧化防御系统可能参与 ROS 的清除。在这篇综述中，我们总结了 ROS 的生物学作用的主要发现，这些作用可能有助于 COPD 的发展，并对抗这种疾病进展的细胞保护机制。
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