title: [The levels of oxidant and antioxidant in patients with COPD].
abstract: It is determinate that oxidant-antioxidant imbalance is responsible for pathogenesis of chronic obstructive pulmonary disease (COPD) and smoking is playing a part in the pathogenesis. It was aimed to investigate the oxidant-antioxidant imbalance in smokers and pathogenesis of COPD and their relations with lung functions. This study was done prospectively in Firat University Medical Faculty, Department of Chest Diseases. The levels of plasma malonyldialdehyde (MDA), erythrocyte reducted glutathione (GSH) and erythrocyte catalase were studied in 20 patients with COPD, in 20 smokers and in 20 nonsmokers. All of the cases were male. Pulmonary function tests were done to all cases and the predicted values of FEV1, FVC, and FEV1/FVC were measured. The levels of plasma MDA: 1.44 +/- 0.23 nmol/mL, 1.51 +/- 0.27 nmol/mL and 1.29 +/- 0.13 nmol/mL, the levels of erythrocyte GSH: 0.33 +/- 0.13 micromol/g.Hb, 0.34 +/- 0.17 micromol/g.Hb and 0.44 +/- 0.14 micromol/g.Hb and the levels of catalase were 22.82 +/- 17.47 k/g.Hb, 32.88 +/- 22.36 k/g.Hb and 55.73 +/- 26.56 k/g.Hb in patients with COPD, smokers and healthy nonsmokers respectively. There was no significance in each three parameters between smokers and patients with COPD. A significant difference was observed in each three parameters between nonsmokers and patients with COPD (MDA: p= 0.001, GSH: p= 0.028 and catalase: p< 0.001) and between smokers and nonsmokers (MDA: p= 0.035, GSH: p= 0.016 and catalase: p= 0.005). In all three groups, no significant correlation was found between FEV1 (predicted %), FEV1/FVC (predicted %) and the values of erythrocyte catalase, GSH and plasma MDA. In this study, there was an oxidant-antioxidant imbalance systemically in smokers and in patients with COPD. However, decreasing in the antioxidant capacity and/or increasing in the oxidant capacity either not correlate with spirometric measurements of airway obstruction in smokers or in patients with COPD were observed. We concluded that the use of cigarette increased oxidative stress by causing plasma lipid peroxidation and imbalance in erythrocyte antioxidant capacity.
authors.affiliation: Batman Goverment Chest Hospital, Batman, Turkey.
authors.forename: Elif
authors.initials: E
authors.lastname: Altuntaş
authors.forename: Teyfik
authors.initials: T
authors.lastname: Turgut
authors.forename: Necip
authors.initials: N
authors.lastname: Ilhan
authors.forename: Figen
authors.initials: F
authors.lastname: Deveci
authors.forename: Hamdi M
authors.initials: HM
authors.lastname: Muz
authors.forename: Ilhami
authors.initials: I
authors.lastname: Celik
mesh_terms: D000368:Aged; D000975:Antioxidants / Q000378:metabolism*; D016022:Case-Control Studies; D002374:Catalase / Q000378:metabolism; D004912:Erythrocytes / Q000378:metabolism; D005978:Glutathione / Q000378:metabolism; D006801:Humans; D008297:Male; D008315:Malondialdehyde / Q000097:blood; D008875:Middle Aged; D016877:Oxidants / Q000097:blood*; D011446:Prospective Studies; D029424:Pulmonary Disease, Chronic Obstructive / Q000097:blood*; D012129:Respiratory Function Tests; D012907:Smoking
chemical_list: D000975:Antioxidants; D016877:Oxidants; D008315:Malondialdehyde; D002374:Catalase; D005978:Glutathione