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Nutrition and Cancer

Vitamin E Supplementation Does Not Alter Azoxymethane-Induced Colonic Aberrant Crypt Foci Formation in Young or Old Mice¹

Heekyung Chung^*, Dayong Wu^*, Sung Nim Han^*, Raina Gay^*, Barry Goldin, Roderick E. Bronson^**, Joel B. Mason^*, Donald E. Smith^* and Simin Nikbin Meydani^*,2

^* Jean Mayer U.S. Department of Agriculture Human Nutrition Research Center on Aging at Tufts University, Boston, MA; Department of Community Health Nutrition/Infectious Disease Unit, Tufts University School of Medicine, Boston, MA; ^** Department of Biological Science, Tufts University School of Veterinary Medicine, North Grafton, MA; and Department of Pathology, Sackler Graduate School of Biomedical Sciences, Tufts University School of Medicine, Boston, MA

²To whom correspondence should be addressed. E-mail: smeydani{at}hnrc.tufts.edu.

Vitamin E, part of the body’s primary lipid-soluble defense against free radicals and reactive oxygen molecules, has been suggested to reduce the risk for some cancers. However, the role of vitamin E in the etiology and prevention of colon cancer, especially in the highest risk group, the aged, is not clear. Thus, this study was conducted to elucidate the effect of vitamin E supplementation on susceptibility to colon cancer by examining azoxymethane (AOM)-induced aberrant crypt foci (ACF) formation, a surrogate biomarker of colon cancer. Young (3–4 mo) and old (19–20 mo) C57BL/6JNIA mice were fed either a control diet (30 mg dl--tocopheryl acetate/kg diet) or a vitamin E-supplemented diet (500 mg dl--tocopheryl acetate/kg diet) for 16 wk. After 6 wk of dietary supplementation, young and old mice were injected with saline or AOM weekly for 5 wk to receive the same total dose of AOM (2.2 mg) and killed 10 wk after the first AOM injection. Vitamin E supplementation had no effect on the number of AOM-induced ACF in young or old mice. In addition, vitamin E supplementation did not have an effect on splenocyte interferon-, interluekin-6 and tumor necrosis factor- levels, natural killer cell killing activity or colonic cell proliferation in young or old mice. Thus, -tocopherol does not seem to affect the initiation and early promotion stages of AOM-induced colon carcinogenesis in young or old mice. Whether vitamin E supplementation might be effective in reducing AOM-induced colon tumors is unclear.

KEY WORDS: • vitamin E • colon cancer • aberrant crypt foci • mice

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