Monika Kmeťová - Sivoňová1, Ľubica Stankovičová1, Marta Vilčková1, Dušan Dobrota1, Mária Kovalská1, Zuzana Tatarková1, Martina Pavlíková1, Ján Kliment2
Introduction and Aims: Reactive oxygen species (ROS) mediated DNA damage in addition to ineffective DNA repair mechanisms are well established lesions common to human cancers. DNA alterations like strand breaks, base modifications and DNA-protein cross linkages are all strongly implicated in the initiation stage of carcinogenesis. Major oxidative DNA damage product 8-oxo-7,8-dihydro-2´-deoxyguanosine (8-oxodG) is regarded as a potential biomarker of mutagenesis consequent to oxidative stress. The aim of the present study was to detect the DNA oxidative damage in prostate cancer and in healthy individuals to understand the mechanism, to monitor participation of the oxidative stress in the process of damage of biologically important molecules and in the process of carcinogenesis. Material and Methods: The study included 20 prostate cancer patients (mean ± SEM: 63.35 ± 1.8 years) and 20 control subjects (mean ± SEM: 65.95 ± 1.8 years) for the analysis of 8-oxodG using a modified single cell gel electrophoresis (Comet assay). The results were analysed with the Student’s paired t-test. Results: The levels of 8-oxodG were significantly higher (p < 0.05) in prostate cancer patients than in controls. There was a positive correlation between the levels of 8-oxodG and serum PSA levels and we have found no correlation between 8-oxodG and Gleason score in prostate cancer patients. Conclusions: Our results demonstrate that an increased rate of oxidative stress might play a role in the pathogenesis of prostate cancer as evidenced by a failure in the oxidant/antioxidant balance in favour of DNA damage.