RESUMO
The aim of this study was to determine the markers of nitric oxide [NO] metabolism [nitritelnitrate [NO2/NO3], nitrotyrosine and peroxynitrite inhibitory activity] in subjects with chronic obstructive pulmonary disease [COPD] and whether they correlate with oxidantlantioxidant system markers, which are glutathione [GSH], vitamin C and thiobarbituric acid reactive substance [TBARS]. Our results showed that, patients with COPD have a lower lung function than normal healthy control. Significant lower GSH levels were observed in the COPD group [3.22 +/- 1.06 micro mol/g Hb] compared with control group [4.83 +/- 1.03 micro mol/g Hb]. Also lower GSH levels were observed in smokers compared to nonsmokers in both groups. Mean levels of serum NO2/NO3 in patients with COPD [77.6 +/- 11.6 micro mol/L] were significantly higher than in healthy control group [26.42 +/- 8.4 micro mol/L] and also higher in smokers compared to nonsmokers. In contrast, peroxy nitrite inhibitory activity was significantly lowered in patients with COPD than normal controls [51.31 +/- 3.1 vs 94.3 +/- 7.1%, at p<0.001] and was also significantly correlated with FEV1 [r=0.591]. Moreover, there was a significant negative correlation between peroxynitrite inhibitory activity and NO2/NO3 levels in COPD patients [r=-0.716]. Nitrotyrosine concentrations were significantly increased in patients with COPD [54.7 +/- 5.2 ng/ml] compared with control group [8.36 +/- 0.71 ng/ml]. Lipid peroxidation levels were significantly higher in patients with COPD than in normal controls [2.01 +/- 0.80 vs 0.62 +/- 0.13 nmol/L]. TBARS levels were also significantly higher in smokers than nonsmokers. In contrast, vitamin C concentrations was significantly lower in patients with COPD than in normal controls [1.11 +/- 0.02 vs 2.19 +/- 0.31 mg/dl]. Our results showed a significant decrease in the peroxynitrite inhibitory activity, GSH and vitamin C and an increase in NO2/NO3, nitrotyrosine, and TBARS levels in patients with COPD compared to healthy controls which may provide some evidence for a potential role of increased NO metabolites production and decreased antioxidant activity in COPD especially in smokers