McCusker K, Hoidal J
Pulmonary Division, University of Tennessee, Memphis.
Am Rev Respir Dis. 1990 Mar;141(3):678-82. doi: 10.1164/ajrccm/141.3.678.
Oxidants from cigarette smoke or those produced by phagocytes are implicated in the pathogenesis of emphysema. We reasoned that augmentation of antioxidant enzymes in cigarette smokers may be important in restricting direct and indirect oxidant damage to alveolar structures. Accordingly, we studied the activities of superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSHPx), in alveolar macrophages (AM) from cigarette smokers and from smoke-exposed hamsters. The activities of these antioxidant enzymes were compared with the activities found in AM from nonsmoking control subjects. The activities of SOD and CAT from AM of smokers and smoke-exposed hamsters were twice that found in control subjects (p less than 0.01), but there was no change in the activity of GSHPx. Using the hamster model, we found that filtration of smoke attenuated the increase in antioxidant activities, and that after smoking cessation, the increased activities had returned to those found with control subjects. An adaptive response was further suggested by prolonged survival of smoke-exposed hamsters in normobaric hyperoxia (O2 greater than 95%). Chronic smoke exposure in humans or hamsters causes increased SOD and CAT activities in AM. This augmented activity may serve as a mechanism to limit oxidant-mediated damage to alveolar structures.
香烟烟雾中的氧化剂或吞噬细胞产生的氧化剂与肺气肿的发病机制有关。我们推断，增强吸烟者体内抗氧化酶的活性对于限制对肺泡结构的直接和间接氧化损伤可能很重要。因此，我们研究了吸烟者和暴露于烟雾中的仓鼠肺泡巨噬细胞（AM）中超氧化物歧化酶（SOD）、过氧化氢酶（CAT）和谷胱甘肽过氧化物酶（GSHPx）的活性。将这些抗氧化酶的活性与非吸烟对照受试者的AM中发现的活性进行了比较。吸烟者和暴露于烟雾中的仓鼠的AM中SOD和CAT的活性是对照受试者的两倍（p小于0.01），但GSHPx的活性没有变化。使用仓鼠模型，我们发现烟雾过滤减弱了抗氧化活性的增加，并且戒烟后，增加的活性已恢复到对照受试者的水平。常压高氧（氧气大于95%）下暴露于烟雾中的仓鼠的长期存活进一步表明了一种适应性反应。人类或仓鼠长期接触烟雾会导致AM中SOD和CAT活性增加。这种增强的活性可能是限制氧化介导的肺泡结构损伤的一种机制。
