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Year : 2012  |  Volume : 8  |  Issue : 2  |  Page : 254-259

Assessment of the redox profile and oxidative DNA damage (8-OHdG) in squamous cell carcinoma of head and neck

1 Immunotoxicology Division, CSIR, Indian Institute of Toxicology Research, Lucknow, India
2 Ch. S.M. Medical University, Lucknow, India
3 Ch. Charan Singh University Meerut, India

Correspondence Address:
Shashi Khandelwal
Scientist F and Head, CSIR - Indian Institute of Toxicology Research, 80 Mahatma Gandhi Marg, Lucknow 226001
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Source of Support: None, Conflict of Interest: None

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Background: In developing countries especially in south Asia, there are growing habits of consumption of tobacco and its products in various forms. These are known to generate a strong free radical environment and when the free radicals overwhelm the antioxidant system, they may lead to degeneration of cellular components and mutations. Aim: The aim of this study is to assess the levels of oxidative stress determinants, which may be one of the critical factors in head and neck cancer development. Materials and Methods: This study included 100 consenting SCCHN patients and 90 matched healthy controls and we assessed the total antioxidant capacity (TAC), glutathione (GSH), free radicals (RNS, ROS) and oxidative DNA adduct (8-OHdG). Results: We observed a substantial rise in reactive oxygen species (ROS, ~3.0-fold) and reactive nitrogen species (RNS, ~1.7-fold), together with significant lowering in TAC (~1.2-fold) and GSH (~1.7-fold) was observed. The 8-OHdG levels were also found to be significantly (P < 0.05) higher in patients in comparison to controls. Pearson's correlation between blood ROS and GSH were found to be negatively correlated -0.38 (P < 0.01) and RNS and DNA damage positively correlated 0.44 (P < 0.01). Conclusion: Our present results demonstrate significant Redox imbalance in cancer patients suggesting their paramount importance in the development of SCCHN. The 8-OHdG could be the potential biomarker for evaluating risk of SCCHN. To develop new approaches of SCCHN prevention, there is a need of detailed study and better understanding of the molecular mechanisms underlying oxidative stress and DNA damage.

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