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Submitted to: Journal of Federation of American Societies for Experimental Biology
Publication Type: Abstract Only Publication Acceptance Date: 4/11/2003 Publication Date: N/A Citation: N/A Interpretive Summary: Technical Abstract: The purpose of the current studies was to investigate the effect of different amounts and chemical forms of Se on putative risk factors for colon cancer susceptibility in rats. Wistar rats (n=12/diet) were fed a Se-deficient Torula yeast based diet or the diet supplemented with 2.0 ug Se/g diet as selenite, selenomethionine or Se-methylselenocysteine. These four diets resulted in colonic mucosal cell lipid peroxidation of 406±65, 357±36, 254±26 and 255±22 nmol malondialdehyde/g protein; fecal water alkaline phosphatase activity (an indicator of epithelial cell lysis) of 0.58±0.07, 0.42±0.04, 0.37±0.06 and 0.57±0.05 U/ml and mucosal cell proliferation of 3836±1232, 646±302, 2702±472 and 2896±890 dpm 3H thymidine/mg DNA, respectively (all p<0.05). In a follow up study, the same diets (n=6/diet), resulted in mucosal cell proliferation of 5597±1384, 3031±741, 1965±232 and 2435±647 dpm 3H thymidine/mg DNA (p<0.02), and a free radical generating capacity of the luminal contents of the cecum chyme of 236±11, 162±19, 136±16 and 161±22 umol/g dry wgt, respectively (p<0.009), without affecting the free radical generating capacity of the feces. These results suggest that deficient dietary Se adversely affects putative risk factors for colon cancer susceptibility in rats. |
