title: Selenium (Se) from high-selenium broccoli is utilized differently than selenite, selenate and selenomethionine, but is more effective in inhibiting colon carcinogenesis.
abstract: The reduction in incidence of chemically-induced colon cancer by foods high in selenium (Se) was investigated in Fisher-344 rats. The foods used were high-Se broccoli (produced in a greenhouse by addition of selenate to the media surrounding the plant roots) and a processed high-Se wheat product (made by milling high-Se wheat purchased from a seleniferous area). Weanling rats were fed diets containing different amounts of Se from these foods or from selenium salts (selenite and selenate). Early in the experiment the animals were injected with a chemical carcinogen. After 11 weeks on diets animals were killed and the colons examined for preneoplastic lesions (aberrant crypts foci, ACF). ACF were significantly reduced in animals fed supra-nutritional amounts of Se from broccoli, despite the finding that Se from broccoli was poorly bioavailable. Supra-nutritional amounts of Se from high-Se processed wheat also significantly reduced aberrant crypts (AC), although pure selenomethionine, (the predominant chemical form of Se in wheat), did not significantly reduce AC. These results emphasize the need to study Se in food forms, and not extrapolate from previous studies using pure chemical forms in cancer inhibition studies. They also demonstrate that foods with high Se bioavailability are not necessarily the most efficacious for cancer incidence reduction.
authors.affiliation: United States Department of Agriculture, Agricultural Research Service, Grand Forks Human Nutrition Research Center, ND 58202, USA. jfinley@gfhnrc.ars.usda.gov
authors.forename: J W
authors.initials: JW
authors.lastname: Finley
authors.forename: C D
authors.initials: CD
authors.lastname: Davis
mesh_terms: D000818:Animals; D016588:Anticarcinogenic Agents / Q000493:pharmacokinetics / Q000494:pharmacology*; D001937:Brassica; D002273:Carcinogens; D003106:Colon / Q000187:drug effects / Q000473:pathology*; D003110:Colonic Neoplasms / Q000139:chemically induced / Q000517:prevention & control*; D005786:Gene Expression Regulation / Q000187:drug effects; D005979:Glutathione Peroxidase / Q000235:genetics; D008099:Liver / Q000187:drug effects / Q000378:metabolism; D008297:Male; D011506:Proteins / Q000235:genetics; D051381:Rats; D011916:Rats, Inbred F344; D064586:Selenic Acid; D012643:Selenium / Q000378:metabolism* / Q000494:pharmacology*; D018036:Selenium Compounds / Q000493:pharmacokinetics / Q000494:pharmacology; D012645:Selenomethionine / Q000493:pharmacokinetics / Q000494:pharmacology; D051140:Selenoproteins; D018038:Sodium Selenite / Q000493:pharmacokinetics / Q000494:pharmacology; D014908:Triticum; D000094765:Glutathione Peroxidase GPX1
chemical_list: D016588:Anticarcinogenic Agents; D002273:Carcinogens; D011506:Proteins; D018036:Selenium Compounds; D051140:Selenoproteins; D012645:Selenomethionine; D005979:Glutathione Peroxidase; D012643:Selenium; D018038:Sodium Selenite; D064586:Selenic Acid; D000094765:Glutathione Peroxidase GPX1