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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.

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The present study evaluated the modulatory potential of selenium on colonic surface abnormalities and membrane fluidity changes following 1,2-dimethylhydrazine (DMH) induced colon carcinogenesis. Rats were segregated into four groups viz., normal control, DMH treated, selenium treated, and DMH + selenium treated. Initiation of molecular events leading to colon carcinogenesis was started following weekly subcutaneous injections of DMH (30 mg/Kg body weight) for 10 weeks. Selenium in the form of sodium selenite was supplemented to rats at a dose level of 1 PPM in drinking water, ad libitum for the entire duration of the study. Brush border membranes were isolated from the colon of rats and the viscosity as well as fluidity parameters were assessed using the membrane extrinsic fluorophore pyrene. DMH treatment resulted in a significant increase in lipid peroxidation. Reduced glutathione levels (GSH) and the activities of glutathione reductase (GR), glutathione transferase (GST), superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) were found to be significantly decreased following DMH treatment. On the other hand, supplementation with selenium to DMH treated rats resulted in a significant decrease in the levels of lipid peroxidation but caused a significant increase in the levels of GSH as well in the activities of GR, GST, SOD, CAT, and GPx. The results further, demonstrated a marked decrease in membrane microviscosity following DMH treatment. On the other hand, a significant increase was observed in the excimer/monomer ratio and fluidity parameter of DMH treated rats when compared to normal control rats. However, the alterations in membrane microviscosity and the fluidity parameters were significantly restored following selenium treatment. Further, histological as well as colon surface alterations were also observed following DMH treatment, which however were greatly prevented upon selenium co-administration. The study, therefore, concludes that selenium proves as a useful in modulating the colonic surface abnormalities and membrane stability following DMH induced colon carcinogenesis.

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