Oxidative modification of proteins in pediatric cystic fibrosis with bacterial infections.

Pseudomonas aeruginosa and Staphylococcus aureus cause chronic lung infection in cystic fibrosis (CF) patients, inducing chronic oxidative stress. Several markers of plasma protein oxidative damage and glycoxidation and activities of erythrocyte antioxidant enzymes have been compared in stable CF patients chronically infected with Pseudomonas aeruginosa (n = 12) and Staphylococcus aureus (n = 10) in relation to healthy subjects (n = 11). Concentration of nitric oxide was also measured in the exhaled air from the lower respiratory tract of patients with CF. Elevated glycophore (4.22 ± 0.91 and 4.19 ± 1.04 versus control 3.18 ± 0.53 fluorescence units (FU)/mg protein; P < 0.05) and carbonyl group levels (1.9 ± 0.64, 1.87 ± 0.45 versus control 0.94 ± 0.19 nmol/mg protein; P < 0.05) as well as increased glutathione S-transferase activity (2.51 ± 0.88 and 2.57 ± 0.79 U/g Hb versus 0.77 ± 0.16 U/g Hb; P < 0.05) were noted in Pseudomonas aeruginosa and Staphylococcus aureus infected CF. Kynurenine level (4.91 ± 1.22 versus 3.89 ± 0.54 FU/mg protein; P < 0.05) was elevated only in Staphylococcus aureus infected CF. These results confirm oxidative stress in CF and demonstrate the usefulness of the glycophore level and protein carbonyl groups as markers of oxidative modifications of plasma proteins in this disease.