Total nitrite/nitrate in expired breath condensate of patients with asthma

AbstractProduction of nitric oxide (NO) is generally increased during inflammatory diseases including asthma. The eventual fate of NO is oxidation to nitrite (NO2) and nitrate (NO3), both of which are end-products of NO metabolism. Hydrogen Peroxide (H2O2) is increased in exhaled breath condensate of asthmatic subjects and may be used as a non-invasive marker of oxidative stress. NO has in some cases been shown to attenuate oxidant-induced lung injury. Total NO2/NO3concentration and H2O2levels were measured in expired breath condensate in 50 clinically stable asthmatics [all males, all atopics, mean age 22 (3) SD yrs, forced expiratory volume in 1 sec (FEV1) 91(10)% predicted, PD20to histamine 0·262 (0·16) mg 20 on inhaled steroids, 20 smokers, all steroid-naive] and in 10 normal, non-atopic subjects [all males, age 23 (4) yrs, FEV1101 (14)% predicted, PD20to histamine 1·3 (0·55) mg]. NO2/NO3levels were significantly higher in patients with asthma than in normal subjects (1·08, 95% CI 0·86–1·3 μMvs. 0·6; 95% CI 0·46–0·8,P <0·001). Patients who were on inhaled steroids had significantly lower values compared to steroid-naive (0·71, 95% CI 0·55–0·87 μMvs. 133, 95% CI 1–1·65 μM, P<0·001). Similar results were observed between smokers and non-smokers (1·11, 95% CI 0·74–1·47 μMvs. 1·77, 95% CI 1·1–2·4 μM,P <0·0001). There was a significant positive correlation between NO2/NO3levels and H2O2concentration in expired breath condensate (r=0·48, P