Increased hydrogen peroxide and thiobarbituric acid-reactive products in expired breath condensate of asthmatic patients.

Symptoms of bronchial asthma are a manifestation of airway inflammation. Circulatory leucocytes (predominantly eosinophils, mast cells and neutrophils), release inflammatory mediators, including reactive oxygen species, i.e. superoxide anion which is dismutated to hydrogen peroxide (H2O2). Neutrophils from asthmatics generate greater amounts of these species than those of healthy subjects. Some of the H2O2 and thiobarbituric acid-reactive products (TBARs) can evaporate from alveolar lining fluid, and could be expired from the airways of asthmatics. In this study, therefore, we determined whether asthmatic patients exhale more H2O2 and TBARs than healthy subjects. We examined 10 healthy subjects as a control group and 21 asthmatic subjects. In asthmatic subjects, forced expiratory volume in one second (FEV1), was 68+/-9% of predicted value, peak expiratory flow rate (PEFR) was 65+/-8% pred, and bronchial reversibility was 34+/-5% of prebronchodilated FEV1. The mean H2O2 level measured spectrofluorimetrically in the expired breath condensate of asthmatic subjects was 26 fold higher than that in healthy controls (0.26+/-0.29 vs 0.01+/-0.03 nM; p<0.05). The concentration of TBARs in breath condensate was also higher in asthmatic patients compared with nonasthmatics (0.073+/-0.071 vs 0.004+/-0.009 nM; p<0.05). There was a significant correlation between H2O2 level and concentration of TBARs in asthmatic patients (r=0.74; p<0.01). There was also a strong inverse correlation between H2O2 content of all asthmatics and FEV1% pred (r=-0.63; p<0.005) and PEFR% pred (r=-0.52; p<0.05). We conclude that there are elevated levels of hydrogen peroxide and thiobarbituric acid-reactive products in expired breath condensate of asthmatic patients, and that measurement of these substances in the expired breath condensate could be a simple, noninvasive method that could be used as a biochemical marker of airway inflammation.

[1]  T. Pietras,et al.  Increased content of hydrogen peroxide in the expired breath of cigarette smokers. , 1996, The European respiratory journal.

[2]  M. Kaliner,et al.  Hydrogen peroxide effects on rat mast cell function. , 1994, The American journal of physiology.

[3]  T. Stijnen,et al.  Oxidative epithelial damage produces hyperresponsiveness of human peripheral airways. , 1994, American journal of respiratory and critical care medicine.

[4]  Abraham Wm.  The interaction among granulocyte lipid mediators and the generation of oxygen radicals in antigen-induced airway hyperresponsiveness. , 1994 .

[5]  W. Abraham.  The interaction among granulocyte lipid mediators and the generation of oxygen radicals in antigen-induced airway hyperresponsiveness. , 1994, Advances in prostaglandin, thromboxane, and leukotriene research.

[6]  H. Black,et al.  Expired breath hydrogen peroxide is a marker of acute airway inflammation in pediatric patients with asthma. , 1993, The American review of respiratory disease.

[7]  H. Hämmerle,et al.  Detection of nonvolatile macromolecules in breath. A possible diagnostic tool? , 1993, The American review of respiratory disease.

[8]  M. Kadiiska,et al.  Electron spin resonance spin-trapping investigation into the effects of paraquat and desferrioxamine on hydroxyl radical generation during acute iron poisoning. , 1993, Molecular pharmacology.

[9]  T. Fukuda,et al.  Effect of eosinophil peroxidase on beta-adrenergic receptor density on guinea pig lung membrane. , 1992, Biochemical and biophysical research communications.

[10]  W. Bezwoda,et al.  Persistent neutrophil activation in mild asthma. , 1992, The Journal of allergy and clinical immunology.

[11]  B. Freeman,et al.  Peroxynitrite-induced membrane lipid peroxidation: the cytotoxic potential of superoxide and nitric oxide. , 1991, Archives of biochemistry and biophysics.

[12]  A. B. Kay,et al.  Asthma and inflammation. , 1991, The Journal of allergy and clinical immunology.

[13]  R. Crystal,et al.  Antioxidant macromolecules in the epithelial lining fluid of the normal human lower respiratory tract. , 1990, The Journal of clinical investigation.

[14]  P. Barnes,et al.  Reactive oxygen species and airway inflammation. , 1990, Free radical biology & medicine.

[15]  S. Varma,et al.  Excretion of hydrogen peroxide in human urine. , 1990, Free radical research communications.

[16]  D. Janero,et al.  Malondialdehyde and thiobarbituric acid-reactivity as diagnostic indices of lipid peroxidation and peroxidative tissue injury. , 1990, Free radical biology & medicine.

[17]  L. Borish,et al.  Asthmatic patients have neutrophils that exhibit diminished responsiveness to adenosine. , 1989, The American review of respiratory disease.

[18]  A. Nahum,et al.  Increased hydrogen peroxide in the expired breath of patients with acute hypoxemic respiratory failure. , 1989, Chest.

[19]  M. Habib,et al.  Ethane production rate in rats exposed to high oxygen concentration. , 1988, The American review of respiratory disease.

[20]  Buist As.  Standardization of spirometry. , 1987 .

[21]  M. Snider,et al.  Increased N-pentane Excretion in Humans: A Consequence of Pulmonary Oxygen Exposure , 1986, Anesthesiology.

[22]  Cockcroft Dw.  Bronchial inhalation tests. I. Measurement of nonallergic bronchial responsiveness. , 1985 .

[23]  D. Cockcroft.  Bronchial inhalation tests. I. Measurement of nonallergic bronchial responsiveness. , 1985, Annals of allergy.

[24]  D. Tierney,et al.  Poor correlation between oxygen toxicity and activity of glutathione peroxidase. , 1983, Experimental lung research.

[25]  M. Baggiolini,et al.  Assay of H2O2 production by macrophages and neutrophils with homovanillic acid and horse-radish peroxidase. , 1983, Journal of immunological methods.

[26]  K. Yagi,et al.  A simple fluorometric assay for lipoperoxide in blood plasma. , 1976, Biochemical medicine.