Hanta Ismail, Kocabas Ali, Canacankatan Necmiye, Kuleci Sedat, Seydaoglu Gulsah
Department of Chest Disease, School of Medicine, Cukurova University, 01330, Balcali, Adana, Turkey.
Lung. 2006 Mar-Apr;184(2):51-5. doi: 10.1007/s00408-005-2561-4.
The goal of this study was to evaluate the role of oxidant-antioxidant balance in the pathogenesis of COPD. We included 30 healthy nonsmokers [24 male, 6 female; mean age (yr) +/- SD: 62.4 +/- 9.3], 30 healthy smokers [27 male, 3 female; mean age (yr) +/- SD: 58.7 +/- 6.0], 71 patients with stable COPD [68 male, 3 female; mean age (yr) +/- SD: 63.5 +/- 7.9], and 31 patients with COPD exacerbation [30 male, 1 female; mean age (yr) +/- SD: 64.2 +/- 7.3]. In all study groups the peripheral venous blood samples were taken for plasma malonyldialdehyde (MDA), a parameter of lipid peroxidation caused by the oxidants, and erythrocyte superoxide dismutase (SOD), an antioxidant enzyme. The mean plasma MDA level was higher in healthy smokers and in patients with COPD than in healthy nonsmokers (p < 0.05), and erythrocyte SOD enzyme activity in patients with COPD exacerbation (1048.2 +/- 226.5 Ug/Hb) was significantly higher than in healthy nonsmokers (947.9 +/- 198.0 Ug/Hb) (p < 0.05). Although mean erythrocyte SOD enzyme activity in healthy smokers and patients with stable COPD was higher than in healthy nonsmokers, the difference was not statistically significant. We found that healthy smokers and stable and exacerbated COPD patients had an impairment in oxidant-antioxidant balance. We suggested that new therapeutic interventions, which may repair the impaired oxidant-antioxidant balance in COPD, are needed to prevent the development of COPD.
