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

Abstract

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