Abstract—Solid tumors show areas of differential blood supply due to decreasing vascularisation from periphery towards the core. As a result, a gradient of oxygen is formed such that internal areas with low oxygen tension lead to altered physiochemical conditions. This state of low oxygen- called hypoxia- is gaining interest due to a large scale shift in metabolism of the tumor cells. Reactive Oxygen Species (ROS) thus produced cause extensive DNA damage in hypoxic core regions, exacerbating the aggressiveness of cancer by accumulation of mutations. We show how the ubiquitous cellular enzyme Catalase may prevent ROS mediated damage through chelation of metal ions. Metal ions are known to increase oxidative stress in a cell and recent reports implicated involvement of metal ions in controlling p53 function. We propose that chelation therapy in solid tumors can delay the accumulation of mutations by catalase mediated decrease in ROS levels and by rescuing the p53 activity in a cell.

Index Terms—Catalase, chelation, hypoxia, oxidative stress.

The Authors are with Amity Institute of Biotechnology, Amity University, Sec-125 NOIDA, UP, India (e-mail: kartikg.spaceset@gmail.com).

Cite: Kartik Gupta, Akriti Kapoor, Sahil Chaudhary, and Purusharth Mohan, "Oncoprotective Role of Chelation Therapy in Hypoxic Solid Tumors: A Theoretical Model," International Journal of Bioscience, Biochemistry and Bioinformatics vol. 2, no. 2, pp. 76-78, 2012.