During pulmonary inflammation increased amounts of reactive oxygen species (ROS) and reactive nitrogen intermediates (RNI) are produced as a consequence of phagocyte respiratory burst. One of the manifestation of these free radical-mediated processes is lipid peroxidation (LP). The aim of our study was to assess the concentration of lipid peroxidation products (LPPs), conjugated diens (CD) and malondialdehyde (MDA), in patients with active TB. Forty-two patients were enrolled into the study. Half (group I) had advanced TB and were sputum smear-positive. The remainder (group II) had only small radiographical changes and were sputum smear-negative. Serum concentrations of CD and MDA were measured at days 0, 7, 14 and 28 in group I and day 0 in group II. We found that in all patients with active TB CCD (1.0 +/- 0.05A233) and CMDA (2.01 +/- 0.16 nmol dl-1) were significantly elevated compared to healthy controls (0.67 +/- 0.03A233 and 1.36 +/- 0.08 nmol dl-1, respectively) (P < 0.001). The highest levels of LPPs were in patients with advanced TB. These concentrations were stable during the first month of anti-tuberculous therapy. Our data indicated that, as in bacterial pneumonia, LPPs were enhanced in active TB. The levels of LPPs depended on the form of the disease as they were higher in subjects with advanced disease than in those with only small radiographical changes. Further studies are needed to assess the role of antioxidants as adjuvant therapy in patients with pulmonary TB.

Lipid peroxidation, as a well-known index of reactive oxygen species activity, not only in lung biochemistry, is an oxidative process associated with membrane lipid destruction. Also, the oxidative modification of nucleic acids by reactive oxygen species is of remarkable biological importance as it may contribute to malignant conversion, but its exact role in lung cancer biology is still not clear. Our study aimed to investigate the level of lipid peroxidation ex vivo in tumour tissue and lung parenchyma obtained from patients with lung cancer. Forty-two patients with lung cancer were enrolled into the study. During a surgical resection, tumour tissue and lung parenchyma were obtained and concentration of lipid peroxidation products, thiobarbituric acid-reactive substances and Schiff bases, and spontaneous generation of hydrogen peroxide, were measured. The concentration of thiobarbituric acid-reactive substances (P<0.001) in the tumour tissue was higher than that in lung parenchyma. In small cell lung cancer as well as in squamous cell carcinoma patients, a positive correlation between spontaneous generation of hydrogen peroxide in tumour tissue and clinical stage (r = 0.43; r = 0.46; respectively) was found. Our results prove enhanced lipid peroxidation in cancer tissue as compared with matched-lung parenchyma. In small cell lung cancer and squamous cell carcinoma patients, the high level of oxidative stress, expressed as a spontaneous generation of hydrogen peroxide in tumour tissue, was associated with clinical progression of tumour's stage.

Background: Matrix metalloproteinase-9 (MMP-9) and its inhibitor tissue inhibitor of metalloproteinase-1 (TIMP-1) are involved in the pathogenesis of airway inflammation in patients with chronic obstructive pulmonary disease (COPD). However, no study so far has addressed their value as noninvasive biomarkers of airways inflammation. Objective: To evaluate MMP-9 and TIMP-1 concentrations in the exhaled breath condensate (EBC) of patients with stable COPD and also during the exacerbation episode. Methods: EBC and serum samples were collected in 17 stable-phase COPD patients who were current smokers as well as during their first exacerbation episode, and in 22 asymptomatic smokers. EBC and serum levels of MMP-9 and TIMP-1 were measured with ELISA kit. Results: Mean EBC MMP-9 and TIMP-1 levels were higher in patients with stable COPD than in asymptomatic smokers. Exacerbation of COPD increased 2-fold the exhalation of MMP-9 (18.5 ± 10.1 ng/ml vs. 8.9 ± 6.2 ng/ml, p = 0.01) and TIMP-1 (to 41.1 ± 20.4 ng/ml vs. 16.4 ± 6.8 ng/ml, p < 0.001). Both, MMP-9 and TIMP-1 in EBC correlated negatively with FEV₁ (% predicted) at baseline (r = –0.78, p < 0.001 and r = –0.73, p < 0.001) and during the exacerbation episode (r = –0.57, p = 0.02 and r = –0.65, p = 0.005). Similar negative correlations were noted with FVC (% predicted), except for MMP-9 in EBC at exacerbation. Exhaled MMP-9 and TIMP-1 did not correlate with serum concentrations in COPD patients, either at baseline or during exacerbation. Conclusion: Exhaled MMP-9 and TIMP-1 increased during COPD exacerbation and was negatively correlated with spirometric variables, which suggests the usefulness of their measurement in EBC for the monitoring of airways inflammation. However, to better assess their diagnostic or prognostic value larger studies are necessary.

Mycobacteria are the strong stimulators of respiratory burst, resulting in production of reactive oxygen species and nitrogen intermediates. The aim of our study was to assess the concentration of hydrogen peroxide (H(2)O(2)) in expired breath condensate (EBC) and the serum level of interleukin-18 (IL-18) in patients with active pulmonary tuberculosis (TB) before introduction of chemotherapy and after 2 months of treatment. Sixteen patients, current cigarette smokers, with advanced pulmonary TB were enrolled into the study. As a control served two groups: I group--16 asymptomatic cigarette smokers, II group--17 healthy never smoked subjects. The level of H(2)O(2) in EBC was significantly higher in patients with TB (1.3+/-0.7 microM) as compared to cigarette are healthy nonsmoker subjects (0.4+/-0.1 and 0.2+/-0.1 microM, respectively, P<0.05). Two months of treatment significantly decreased the level of H(2)O(2) exhalation in TB patients (0.5+/-0.3 microM) to the value that was not different from that in asymptomatic smokers but was still higher than in never smoked subjects. Serum concentration of IL-18 in TB patients was higher than that found in both control groups either before and after antituberculous treatment (P<0.05). Exhaled H(2)O(2) did not correlate with circulating IL-18 in TB patients before or after treatment. These results demonstrated the occurrence of oxidative stress in the airways of TB patients completely attenuating after 2 months of successful antituberculous treatment.

Background: The aim of the study was to compare markers of local and systemic inflammation in patients with community-acquired pneumonia (CAP) and pneumonia co-existing with lung cancer. Material and methods: We enrolled 17 patients with CAP (Group 1), 14 patients with pneumonia co-existing with lungcancer (Group 2), 24 patients with lung cancer (Group 3) and 16 healthy individuals (Group 4, the control group). We evaluated the concentrations of hydrogen peroxide (H2O2), vascular endothelial growth factor (VEGF) and tumour necrosis factor-alpha (TNF-α) in exhaled breath condensate (EBC) and serum concentrations of VEGF and TNF-α. Results: We found significantly higher EBC concentrations of VEGF and TNF-α in patients with pneumonia co-existing with lung cancer than in CAP patients (317.83 ± 77.78 vs. 30.20 ±6.56 and 1.98 ± 0.13 vs. 0.31 ± 0.05, respectively). Although the EBC concentration of H2O2 in patients with pneumonia co-existing with lung cancer was higher than that in CAP patients (0.96 ± 0.16 vs. 0.66 ± 0.09), the difference was not significant (p > 0.05). In CAP patients, however, we observed significantly higher serum concentrations of both cytokines compared to patients with pneumonia co-existing with lung cancer (VEGF: 1112.62 ± 244.38 vs. 392.9 ± 78.2; TNF-a: 2.6 ± 0.48 vs. 1.6 ± 0.2). Conclusions: Patients with pneumonia co-existing with lung cancer show a distinct tendency towards local oxidative stress and a significantly increased local response compared to CAP patients. On the other hand, systemic inflammation in patients with pneumonia co-existing with lung cancer is markedly reduced compared to patients with CAP