Increased content of thiobarbituric acid-reactive substances and hydrogen peroxide in the expired breath condensate of patients with stable chronic obstructive pulmonary disease: no significant effect of cigarette smoking

AbstractThe imbalance between oxidants and antioxidants is known to play an important role in the pathogenesis of chronic obstructive pulmonary disease (COPD). Cigarette smoking is the most frequent factor responsible for development of COPD by leading to oxidant overload in the lower airways, due to presence of its own oxidants and to recruitment and activation of pulmonary phagocytes.We aimed to determine whether (1) patients with stable COPD have higher thiobarbituric acid-reactive substances (TBARs, an end-product of lipid peroxidation) and H2O2levels in expired breath condensate than healthy subjects who have never smoked; (2) COPD subjects who are current smokers exhale more TBARs and H2O2than COPD ex-smokers and those who have never smoked; and (3) concentration of TBARs correlates with H2O2levels in the breath condensate of COPD patients.The TBAR and H2O2content in expired breath condensate of 17 healthy nonsmoking subjects and 44 patients (11 current smokers, 20 ex-smokers and 13 who had never smoked) with stable COPD [forced expiratory volume in 1s (FEV1) 63·3±16·3% and FEV1reversibility 5·2±4·3% predicted value] was measured spectrofluorimetrically by the thiobarbituric acid and homovanillic acid methods, respectively.The mean concentrations of TBARs and H2O2in the expired breath condensate of COPD subjects were 12 (0·48–0·86μmvs 0·04±0·14μm ;P<0·05) and 10 times (0·48±0·67μmvs 0·05±0·07μm ;P