It has been suggested that recurring oxidative lung injury can contribute to the decline in pulmonary function in these patients.- In our findings, there was also a weak positive correlation between protein carbonyls and the age of the CF patients (n = 51; rs = 0.32; p = 0.02) but not between age and pulmonary function (n = 51; rs = — 0.22; p = 0.12). This may reflect a decreasing antioxidative capacity with age or declining activity of the proteasome.” Previously it was demonstrated that the formation of myeloperoxidase-derived oxidizing and possibly nitrating species within the respiratory tract of subjects with CF may contribute to bronchial injury and respiratory fail-ure. tadanafil
Nevertheless, this study performed on the population of children with CF revealed no correlation between myeloperoxidase activity, neutrophil numbers, and protein carbonylation. Our data directly support the hypothesis that protein oxidation during chronic and excessive neutrophilic inflammation may contribute to the decline of pulmonary function in CF patients. These processes lead to an increase in local concentrations of free oxygen radicals at the sites of inflammation.’ This may result in the most effective defense against pathogens. However, if the pathogens cannot be eliminated as in CF, a high concentration of free radicals locally and an attenuation of antiproteolytic activity may result in lung tissue damage. It is also known that treatment of infective exacerbations in CF patients results in increased plasma levels of some antioxidant vitamins. However, no immediate changes in plasma protein oxidation are observed, while lipid oxidation is decreased. Also, local antioxidative treatment of CF patients with inhaled glutathione for 2 weeks did not change the level of oxidized proteins in the lungs.