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ARS Home » Northeast Area » Boston, Massachusetts » Jean Mayer Human Nutrition Research Center On Aging » Research » Publications at this Location » Publication #146653
Title: VITAMIN E SUPPLEMENTATION DOES NOT ALTER AZOXYMETHANE-INDUCED COLONIC ABERRANT CRYPT FOCI FORMAITON IN YOUNG AND OLD MICE

Author
item CHUNG, HEEKYUNG - HNRCA
item WU, DAYONG - HNRCA
item HAN, SUNG NIM - HNRCA
item GAY, RAINA - HNRCA
item GOLDIN, BARRY - TUFTS U

Submitted to: Journal of Nutrition
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 11/20/2002
Publication Date: 2/1/2003
Citation: CHUNG, H., WU, D., HAN, S., GAY, R., GOLDIN, B. VITAMIN E SUPPLEMENTATION DOES NOT ALTER AZOXYMETHANE-INDUCED COLONIC ABERRANT CRYPT FOCI FORMAITON IN YOUNG AND OLD MICE. JOURNAL OF NUTRITION. 133:528-32,2003.

Interpretive Summary: As we age the risk for developing various chronic diseases, including cancer increases greatly. Colorectal cancer is the second leading cause of death among cancers in the United States, in which free radicals and reactive oxygen species appear to play a role in development. Increased oxidative stress due to free radicals and reactive oxygen species is associated with increasing age, which may be a major factor in the increase incidence of colorectal cancers in the elderly. Vitamin E, a fat-soluble vitamin, which destroys free radicals and reactive oxygen species, may play a vital role in preventing colorectal cancer. To test the hypothesis that Vitamin E may aid in preventing colorectal cancer, young and old mice were fed either a control diet containing 30 mg dl-alpha-tocopheryl acetate/kg diet or a vitamin E supplemented diet containing 500 mg dl-alpha-tocopheryl acetate/kg diet. After six weeks of dietary supplementation the mice were injected with saline as a negative control or with Azoxymethane (AOM), a chemical stimulator of colon cancer. To determine the development of colon cancer, aberrant crypt foci (ACF) formation, a known biomarker of colon cancer, were counted, splenocyte cytokine analysis, natural killer cell activity, and cell proliferation all immune status markers were also analyzed. Supplementation with vitamin E had no effect on the presence of AOM-induced aberrant crypt formation, splenocyte cytokine analysis, natural kill cell activity, or cell proliferation. This study indicates that vitamin E does not play a pivotal role in preventing the initiation of colon cancer; however further research is still necessary to determine the role vitamin E may play in more advanced stages of colon cancer.

Technical 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-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 (IFN)-g, interleukin (IL)-6, and tumor necrosis factor (TNF)-alpha levels, natural killer (NK) 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 remains unclear.