Rahman I, MacNee W
Unit of Respiratory Medicine, Rayne Laboratory, University of Edinburgh, Scotland.
Free Radic Biol Med. 1996;21(5):669-81. doi: 10.1016/0891-5849(96)00155-4.
An imbalance between oxidants and antioxidants has been considered in the pathogenesis of smoking-induced lung diseases, such as chronic obstructive pulmonary disease (COPD), particularly emphysema. Recent evidence indicates that increased neutrophil sequestration and activation occurs in the pulmonary microvasculature in smokers and in patients with COPD, with the potential to release reactive oxygen species (ROS). ROS generated by airspace phagocytes or inhaled directly from the environment also increase the oxidant burden and may contribute to the epithelial damage. Although much research has focused on the protease/antiprotease theory of the pathogenesis of emphysema, less attention has been paid to the role of ROS in this condition. The injurious effects of the increased oxidant burden in smokers and in patients with COPD are opposed by the lung antioxidant defences. Hence, determining the mechanisms regulating the antioxidant responses is critical to our understanding of the role of oxidants in the pathogenesis of smoking-induced lung disease and to devising future strategies for antioxidant therapy. In this article we have reviewed the evidence for the presence of an oxidant/antioxidant imbalance in smoking-induced lung disease and its relevance to therapy in these conditions.
氧化剂与抗氧化剂之间的失衡已被认为与吸烟所致肺部疾病的发病机制有关，如慢性阻塞性肺疾病（COPD），尤其是肺气肿。最近的证据表明，吸烟者和慢性阻塞性肺疾病患者的肺微血管中会出现中性粒细胞滞留和活化增加，这有可能释放活性氧（ROS）。肺泡吞噬细胞产生的或直接从环境中吸入的活性氧也会增加氧化剂负荷，并可能导致上皮损伤。尽管许多研究都集中在肺气肿发病机制的蛋白酶/抗蛋白酶理论上，但活性氧在这种疾病中的作用却较少受到关注。吸烟者和慢性阻塞性肺疾病患者氧化剂负荷增加所产生的有害影响会受到肺抗氧化防御机制的抵抗。因此，确定调节抗氧化反应的机制对于我们理解氧化剂在吸烟所致肺部疾病发病机制中的作用以及制定未来抗氧化治疗策略至关重要。在本文中，我们回顾了吸烟所致肺部疾病中存在氧化剂/抗氧化剂失衡的证据及其与这些疾病治疗的相关性。
