Brief Article
Copyright ©2009 Baishideng. All rights reserved.
World J Gastrointest Oncol. Oct 15, 2009; 1(1): 74-81
Published online Oct 15, 2009. doi: 10.4251/wjgo.v1.i1.74
Selenium as a chemopreventive agent in experimentally induced colon carcinogenesis
Fereshteh Ezzati Ghadi, Abdollah Ramzani Ghara, Shalmoli Bhattacharyya, Devinder Kumar Dhawan
Fereshteh Ezzati Ghadi, Abdollah Ramzani Ghara, Devinder Kumar Dhawan, Department of Biophysics, Basic Medical Sciences Block, Panjab University, Chandigarh, PIN-160014, India
Shalmoli Bhattacharyya, Department of Biophysics, Post graduate Institute of Medical Education and Research, Chandigarh 160014, India
Author contributions: Ghadi FE and Ghara AR contributed equally to this work; Dhawan DK and Bhattacharyya S designed the research; Ghadi FE and Ghara AR performed the research; Ghadi FE and Ghara AR contributed new reagents tools/analytic; Ghadi FE and Ghara AR analyzed the data; Ghadi FE wrote the paper.
Correspondence to: Devinder Kumar Dhawan, PhD, Professor, Department of Biophysics, Basic Medical Sciences Block, Panjab University, Chandigarh, PIN-160014, India.
Telephone: +91-172-2534121 Fax: +91-172-2534118
Received: February 21, 2009
Revised: March 10, 2009
Accepted: March 17, 2009
Published online: October 15, 2009

AIM: To elucidate the chemopreventive efficacy of selenium during experimentally induced colon carcinogenesis.

METHODS: Thirty-two male wistar rats were divided into four groups: group I (normal control); group II [1,2-dimethylhydrazine (DMH) treated]; group III (selenium treated); and group IV (DMH + selenium treated). Groups II and IV were given subcutaneous injections of DMH (30 mg/kg body weight) every week for 20 wk. Selenium, in the form of sodium selenite, was given to groups III and IV at 1 ppm in drinking water ad libitum for 20 wk. At the end of the study, rats were sacrificed and their colons were analyzed for the development of tumors, antioxidant enzyme levels and histological changes.

RESULTS: 100% of the DMH treated rats developed tumors, which was reduced to 60% upon simultaneous selenium supplementation. Similarly, tumor multiplicity decreased to 1.1 following selenium supplementation to DMH treated rats. Levels of lipid peroxidation, glutathione-S-transferase, superoxide dismutase (SOD), catalase, and glutathione peroxidase (GPx) decreased following DMH treatment, whereas levels of glutathione (GSH) and glutathione reductase (GR) significantly increased in DMH treated rats. Selenium administration to DMH treated rats led to an increase in the levels of lipid peroxidation, SOD, catalase, glutathione-S-transferase and GPx, but decreased the levels of GSH and GR. Histopathological studies on DMH treated rats revealed dysplasia of the colonic histoarchitecture, which showed signs of improvement following selenium treatment.

CONCLUSION: The study suggests the antioxidative potential of selenium is a major factor in providing protection from development of experimentally induced colon carcinogenesis.

Keywords: Colon cancer, Selenium, Antioxidant enzyme, Histopathology, Dimethylhydrazine