Elsevier

Respiratory Medicine

Volume 93, Issue 6, June 1999, Pages 389-396
Respiratory Medicine

Original Article
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

https://doi.org/10.1053/rmed.1999.0574Get rights and content
Under an Elsevier user license
open archive

Abstract

The 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 1 s (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 (0·48–0·86 μmvs 0·04±0·14 μm ;P<0·05) and 10 times (0·48±0·67 μmvs 0·05±0·07 μm ;P<0·005) higher than in healthy controls. Current smokers with COPD did not exhale more H2O2than COPD ex-smokers and those who had never smoked. TBARs levels shared only a tendency to be higher in the breath condensate of smoking COPD subjects than in that of ex-smokers (0·92±1·49 μmvs 0·35±0·44 μm) and of COPD subjects who had never smoked (0·92±1·49 μmvs 0·30±0·53 μm). No correlation was found between TBAR and H2O2levels in the whole COPD group. These variables did not correlate with cigarette smoking status and the time from smoking cessation.

Subjects with stable COPD exhibit increased lipid peroxidation and H2O2generation in the airways. Current cigarette smoking does not distinguish COPD subjects with respect to TBARs and H2O2exhalation.

Cited by (0)

f1

Correspondence should be addressed to: D. Nowak, Department of Pneumology and Allergology, Medical University of Łodz, Kopcinskiego str. 22, 90-153 Łodz, Poland. Fax (48 42) 678 21 29.