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Regular Article| Volume 95, ISSUE 8, P649-654, August 2001

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

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      Abstract

      Production 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) Math Eq 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 μMath Eqvs. 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 μMath Eqvs. 133, 95% CI 1–1·65 μMath Eq, P<0·001). Similar results were observed between smokers and non-smokers (1·11, 95% CI 0·74–1·47 μMath Eqvs. 1·77, 95% CI 1·1–2·4 μMath Eq,P <0·0001). There was a significant positive correlation between NO2/NO3levels and H2O2concentration in expired breath condensate (r=0·48, P<0·0001). No correlation was observed between NO2/NO3levels, airway obstruction and bronchial hyper-reactivity as assessed by PD20to histamine. Total NO2/NO3levels in expired breath condensate are raised in patients with stable asthma and are significantly related to oxidative stress as assessed by H2O2concentration. Measurement of expired breath NO2/NO3and H2O2levels may be clinically useful in the management of oxidation and inflammation mediated lung injury.

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