Free radicals hasten head and neck cancer risk

Abstract

Background:Free radicals such as reactive oxygen species (ROS), which induce oxidative stress, are the main contributors to head and neck carcinogenesis (HNC). The present study was conducted with the aim to assess the oxidant/antioxidant status and DNA damage analysis in head and neck cancer/control patients.Materials and Methods:This prospective study was conducted on 60 patients with biopsy-proven HNC and 17 patients of head and neck disease (HND). The total antioxidant status (TAS), total oxidant status (TOS), and oxidative stress index (OSI) were determined by novel automatic colorimetric methods from tissue homogenate. DNA damage analysis was determined by single cell gel electrophoresis (SCGE).Results:The mean age of the study cohort was 46.65 ± 14.84 years for HNC patients, while it was 49.41 ± 13.00 years for HND patients. There were no significant differences found between the two groups with respect to demographic presentation except tobacco addiction. The association between oxidative stress parameters and DNA damage analysis with study group revealed the following. (A) DNA damage - tissue homogenate TOS and OSI were significantly higher in HNC subjects than in HND (16.06 ± 1.78 AU vs 7.86 ± 5.97 AU, P < 0.001; 53.00 ± 40.61 vs 19.67 ± 21.90, P < 0.01; 7.221 ± 5.80 vs 2.40 ± 2.54, P < 0.01, respectively), while TAS was significantly decreased. (B) Aggressive histological features were identified, more commonly with higher TOS and lower TAS [probability (P) = 0.002, relative risk (RR) = 11.838, 95% confidence interval CI = 2.514-55.730 and P = 0.043, RR = 0.271, 95% CI = 0.077-0.960, respectively].Conclusion:The increase in free radicals may be the event that led to the reduction of antioxidant status in HNC, thus explaining the oxidative damage of DNA and the severity of disease. Increased OSI represents a general mechanism in its pathogenesis.

Glutathione peroxidase (GPx) and superoxide dismutase (SOD) activity in patients with diabetes mellitus type 2 infected with Epstein-Barr virus

“…These findings are in agreement with other researches outcomes [5,8,[24][25][26][27][28]. Lowered activity of these enzymes might be explained by the depletion of antioxidant defense system following the overgeneration of free radicals [29,30]. In diabetic patients glucose autooxidation results in formation of hydrogen peroxide which inactivates SOD.…”

Glutathione Peroxidase (GPx) and Superoxide Dismutase (SOD) in Oropharyngeal Cancer Associated with EBV and HPV Coinfection

“…Decreased antioxidant defense with increased oxidative stress was reported in patients with oral cavity cancer [40]. According to some reports, a lowered level of antioxidant enzymes may be crucial in lesion progression and can lead to the development of oxidative stress [41,42]. Our present study revealed significantly decreased GPx and SOD activity in patients with oropharyngeal cancer with HPV/EBV coinfection in relation to a single viral infection.…”

“…In another study available in the literature performed in HNC patients, poorly and moderately-differentiated tumors were identified more frequently with lower total antioxidant status (TAS). The authors also found increased damage of DNA in cancer patients and supposed that it may be connected with insufficient antioxidant capacity and excessive ROS generation which contributes to the pathogenesis of cancer in HNC patients [42].…”

“…As some studies revealed, decreased antioxidant enzyme activity may also be connected with an advanced stage of malignant lesion and with the lowering level of histological differentiation of HNC tumor [42,44]. Srivastava et al [45] documented lower values of, e.g., SOD and GPx in oral cancer patients with stage II, III, and IV according to TNM classification.…”

Association of Oxidative Stress and Production of Inflammatory Mediators Matrix Metalloproteinase-9 and Interleukin 6: Systemic Events in Radicular Cysts

“…The total antioxidant status indicates the ability of antioxidants to scavenge free radicals. The reduced activity of SOD and GPx may further the development of the lesion, resulting in oxidative stress [28]. Non-toxic levels of ROS increase proinflammatory mediators, and enzymes of the extracellular matrix take part in the destruction of apical tissue and the formation of apical lesions [26,29].…”