Submitted to: Meeting Abstract
Publication Type: Abstract Only
Publication Acceptance Date: 5/28/1999
Publication Date: N/A
Citation: N/A Interpretive Summary:
Technical Abstract: Recent studies linking enhanced selenium (Se) intake to decreased incidence of certain cancers have led to suggestions that Se intakes should be increased beyond the current Recommended Dietary Allowance in the United States. Se inhibition of aberrant colon crypt foci (ACF) formation was studied in rats fed diets supplemented with 0 or 2 ug Se/kg diet as selenite, selenate or selenomethionine, and carcinogenesis was induced with 3,2-dimethyl-4-aminobiphenyl (DMABP). ACF were most numerous in the Se deficient animals (4.4+/-0.9); ACF in animals fed 2 ppm selenomethionine were not different from deficient rats (3.1+/-0.7), but were significantly decreased in rats fed 2.0 mg Se/kg diet as selenite (1.5+/-0.3) or selenate (2.2+/-0.4). Accumulation of Se in the colon was apparently not the factor conferring resistance to ACF formation because Se accumulation in the colon was more than two-fold greater in animals fed 2 mg Se/kg diet as selenomethionine (611+/-11) than in animals fed 2 mg Se/kg diet as selenite (251+/-12 mg/kg). Selenite and selenate also significantly reduced the number of DNA adducts in the colon, but not in the liver, by 50-73%, but selenomethionine did not significantly affect DNA adduct formation (p>0.05). Rats fed 2.0 mg Se/kg diet as high-Se broccoli significantly (p<0.05) reduced ACF in the total colon and rectum (p=0.05) and in the descending colon (p=0.04), as compared to rats fed Se as selenate. These data show that dietary Se is protective against ACF in rats with chemically-induced carcinogenesis and the protective effect is partially determined by the chemical form of the dietary Se.