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-alpha-
tocopheryl acetate/kg diet) or a
vitamin E-supplemented diet (500 mg dl-alpha-
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-gamma, interluekin-6 and
tumor necrosis factor-alpha levels, natural killer cell killing activity or colonic cell proliferation in young or old mice. Thus,
alpha-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.