DNA damage and antioxidant capacity in COPD patients with and without lung cancer.

BACKGROUND AND OBJECTIVE: Chronic obstructive pulmonary disease (COPD) is characterized by chronic inflammation of the lower airways, and COPD patients show two to five times higher risk of lung cancer than smokers with normal lung function. COPD is associated with increased oxidative stress, which may cause DNA damage and lung carcinogenesis. Our aim was to evaluate DNA damage and oxidative stress (lipid peroxidation and antioxidant status) and their relationship in patients with COPD with and without lung cancer. METHODS: We evaluated 18 patients with COPD, 18 with COPD with lung cancer, and 18 controls (former or current smokers). DNA damage was evaluated in peripheral blood lymphocytes using a comet assay; the concentration of malondialdehyde (MDA) and hydrophilic antioxidant performance (HAP) were measured in the plasma. RESULTS: DNA damage was higher in patients with COPD with cancer than in the controls (p = 0.003). HAP was significantly lower in patients with COPD with cancer than in those without cancer and controls. The presence of lung cancer and COPD showed a positive association with DNA strand breaks and the concentration of MDA. CONCLUSION: COPD with lung cancer was associated with elevated DNA damage in peripheral lymphocytes, and cancer and COPD showed a positive correlation with DNA damage. The antioxidant capacity showed a negative association with the interaction COPD and cancer and presence of COPD. The mechanisms underlying the increased incidence of lung cancer in COPD are unknown; DNA damage may be involved. Further research may provide insights into their development and treatment.

Oxidative stress, DNA damage, inflammation and gene expression in occupationally exposed university hospital anesthesia providers.

Considering the importance and lack of data of toxicogenomic approaches on occupational exposure to anesthetics, we evaluated possible associations between waste anesthetic gases (WAGs) exposure and biological effects including oxidative stress, DNA damage, inflammation, and transcriptional modulation. The exposed group was constituted by anesthesia providers who were mainly exposed to the anesthetics sevoflurane and isoflurane (10 ppm) and to a lesser degree to nitrous oxide (150 ppm), and the control group was constituted by physicians who had no exposure to WAGs. The oxidative stress markers included oxidized DNA bases (comet assay), malondialdehyde (high-performance liquid chromatography [HPLC]), nitric oxide metabolites (ozone-chemiluminescence), and antioxidative markers, including individual antioxidants (HPLC) and antioxidant defense marker (ferric reducing antioxidant power by spectrophotometry). The inflammatory markers included high-sensitivity C-reactive protein (chemiluminescent immunoassay) and the proinflammatory interleukins IL-6, IL-8 and IL-17A (flow cytometry). Telomere length and gene expression related to DNA repair (hOGG1 and XRCC1), antioxidant defense (NRF2) and inflammation (IL6, IL8 and IL17A) were evaluated by real-time quantitative polymerase chain reaction. No significant differences (p > .0025) between the groups were observed for any parameter evaluated. Thus, under the conditions of the study, the findings suggest that occupational exposure to WAGs is not associated with oxidative stress or inflammation when evaluated in serum/plasma, with DNA damage evaluated in lymphocytes and leucocytes or with molecular modulation assessed in peripheral blood cells in university anesthesia providers. However, it is prudent to reduce WAGs exposure and to increase biomonitoring of all occupationally exposed professionals.