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Research Article

Influence of extraneous supplementation of zinc on trace elemental profile leading to prevention of dimethylhydrazine-induced colon carcinogenesis

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Pages 493-497 | Received 11 Jan 2010, Accepted 23 Jul 2010, Published online: 16 Sep 2010
 

Abstract

Trace elemental analyses of cancerous tissue is a less explored field of inquiry in cancer research. If the deficiency or excess of a particular trace element can be linked to the cancer, studies can be initiated to see its controlled administration to check the growth of cancer. The present study explored the prophylactic potential of zinc in experimental colon carcinogenesis and also its interaction with other trace metals, which gets altered during the development of colon cancer. Rats were segregated into four groups viz., normal control, dimethylhydrazine (DMH) treated, zinc treated, DMH+zinc treated. Initiation and induction of colon carcinogenesis was achieved through weekly subcutaneous injections of DMH (30 mg/Kg body weight) dissolved in 1 mM EDTA-normal saline (pH 6.5), for 8 and 16 weeks, respectively. Zinc was supplemented at a dose level of 227 mg/L in drinking water, for 8 and 16 weeks. The elemental analyses of colonic samples were carried out using Energy Dispersive X-Ray Fluorescence technique (EDXRF). Zinc administration to DMH treated rats significantly decreased the tumor incidence, tumor multiplicity with simultaneous decrement in tumor size. EDXRF studies revealed that the concentrations of the elements zinc, chromium, manganese and copper were decreased, whereas the concentration levels of iron were found to be increased in the colon tissues following 8 and 16 weeks of DMH treatment. However, zinc supplementation to DMH-treated rats significantly improved the altered levels of elements when compared to DMH-treated animals indicating the chemopreventive role of zinc. In conclusion, DMH induced colon carcinogenesis is accompanied by altered trace element profile and zinc has a positive beneficial effect against chemically-induced colonic carcinogenesis.

Acknowledgements

The authors are thankful to Dr A. K. Sinha, Director, and Dr M. Sudarshan, Senior Scientist, UGC-DAE, Kolkata, for extending valuable help in using the EDXRF facility in the Institute.

Declaration of interest

This work was supported by a financial grant from Indian Council of Medical Research (ICMR), New Delhi, India.

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