Oxidative DNA damage in non small cell lung cancer

Non-small cell lung cancer (NSCLC) is uncontrolled cell proliferation of lung tissue cells and known to be caused by smoking and exposure to various other chemical carcinogens. Oxidative DNA damage caused by oxygen-derived species including free radicals can produce a multiplicity of modifications in DNA such as base and sugar lesions, strand breaks, DNA-protein cross-links and abasic sites. Since this type of damage to DNA can be implicated in the carcinogenesis by causing mutations, the measurement of modifications in DNA from different cancer tissues is essential for understanding the mechanism of carcinogenesis. The aim of this study is to compare the control and cancer tissue DNAs in terms of the oxidative damage and to investigate the correlation between age, smoking, stage and oxidative DNA damage.In this study, DNA samples isolated from tumor and healthy tissues obtained from 29 patients with NSCLC who underwent surgical resection were used. Pathological tissues were investigated in terms of the DNA base and nucleoside damage and compared to healthy control tissues. The level of 8,5-cyclo-2?-deoxyadenosine (S-cdA) were found to be significantly higher in cancer tissues than those in control tissues (p=0.0063). On the other hand 8-hydroxyguanin (8-OH-Gua) and 2,6-diamino-4-hydroxy-5-formamidopyrimidine (FapyGua) levels showed no significant difference between two groups. No significant correlation was found between oxidative DNA damage and age, smoking, clinical or pathological stage.In conclusion we showed, for the first time, the accumulation of wide variety of major products of oxidative damage to DNA in lung tumor tissues. Further research sould deal with prevention of accumulation of oxidative DNA damage and elucidation of DNA repair defects and also possible enhancement of DNA repair in NSCL patients.