ABSTRACT
To study the possible potential of nitric oxide (NO) in the processes of atopic inflammation, the authors evaluated the intensity of nitrosyling and oxidative stresses in the bronchoalvelar lavage fluid and expired air condensate of patients with bronchial asthma (BA). Chronic inflammation was shown to result in an increase in the processes of nitration and oxidation in worsening BA and to reliably correlate with airway NO-producing functions, by explaining the pathological effects of NO due to the formation of 3-nitrotyrosine and malonic dialdehyde with the existing imbalance in NO metabolism, by intensifying nitrosylating stress. In the authors' opinion, nitrosothiols that are required as a NO donor may be rapidly destroyed or virtually do not form so the peroxynitrite-nitrosothiol ratio may predetermine the final effects of NO.
