title: Free radicals hasten head and neck cancer risk: A study of total oxidant, total antioxidant, DNA damage, and histological grade.
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.
  
  
  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].
  
  
  CONCLUSIONS
  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.
authors.forename: A K
authors.initials: AK
authors.lastname: Singh
authors.forename: P
authors.initials: P
authors.lastname: Pandey
authors.forename: M
authors.initials: M
authors.lastname: Tewari
authors.forename: H P
authors.initials: HP
authors.lastname: Pandey
authors.forename: I S
authors.initials: IS
authors.lastname: Gambhir
authors.affiliation: Department of Surgical Oncology, Institute of Medical Sciences, Banaras Hindu University, Varanasi, Uttar Pradesh, India.
authors.forename: H S
authors.initials: HS
authors.lastname: Shukla
mesh_terms: D000328:Adult; D000368:Aged; D000975:Antioxidants / Q000032:analysis*; D015415:Biomarkers / Q000097:blood; D004249:DNA Damage; D004586:Electrophoresis; D005260:Female; D005609:Free Radicals / Q000097:blood; D006258:Head and Neck Neoplasms / Q000235:genetics / Q000473:pathology*; D006801:Humans; D008297:Male; D008875:Middle Aged; D016877:Oxidants / Q000097:blood*; D018384:Oxidative Stress / Q000502:physiology*; D011446:Prospective Studies; D017382:Reactive Oxygen Species
chemical_list: D000975:Antioxidants; D015415:Biomarkers; D005609:Free Radicals; D016877:Oxidants; D017382:Reactive Oxygen Species