Introduction: The primary aim of this research was to evaluate the oxidative stress markers and the level of oxidative DNA damage in the pathogenesis of head and neck cancer. Materials/Methods: Sixty-two subjects matched for age and gender, including 31 patients with head and neck cancer and 31 control patients without cancer symptoms, were enrolled in our study. In our work, the activity of antioxidant enzymes: catalase (CAT), superoxide dismutase (SOD) and glutathione peroxidase (GPX), as well as a total antioxidant status (TAS), were estimated. Additionally, an alkaline comet assay was used to measure the level of DNA damage in the group of patients with head and neck cancer and the group of healthy control patients. These tests were performed on a blood sample with and without prior incubation of dinitratebis (1-phenyl-5-(2-hydroxyphenyl)-3-methyl-N1pyrazol-κN2)cooper(II). Results: Significant increases of SOD, GPX CAT, TAS (P <0.001) were seen in blood from patients with head and neck cancer and prior incubation of cooper (II) component compared to blood from healthy controls without prior incubation of analyzed chemical. Moreover, we did not observe any relationship between the level of DNA damage and the studied component dinitratebis (1-phenyl-5-(2-hydroxyphenyl)-3-methyl-N1pyrazol-κN2)cooper(II) in the group of patients with head and neck cancer or in healthy controls. Discussion: Free radicals such as reactive oxygen species, which induce oxidative stress, may contribute to head and neck carcinogenesis. Therefore, we suggest that modulation of pro-oxidant /antioxidant status might be a relevant target for both prevention and therapy.