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ARS Home » Plains Area » Grand Forks, North Dakota » Grand Forks Human Nutrition Research Center » Healthy Body Weight Research » Research » Publications at this Location » Publication #120944


item Davis, Cindy

Submitted to: Journal of Nutrition
Publication Type: Abstract Only
Publication Acceptance Date: 2/13/2001
Publication Date: N/A
Citation: N/A

Interpretive Summary:

Technical Abstract: Selenium is an essential trace element for human health and has received considerable attention for its possible role as an anticarcinogenic agent. It has been hypothesized that the production of partially methylated forms of selenium may be directly involved in the anticarcinogenic action of selenium. Selenium is enzymatically methylated to mono-, di- and trimethylated metabolites that use S-adenosylmethionine (SAM) as the methyl donor. Arsenic and cytosine DNA methyltransferase compete for methyl donation from SAM. The purpose of these studies was to determine whether changes in the amount and the chemical form of selenium would affect DNA methylation and whether this effect would be modified by arsenic. Caco-2 cells were exposed to 0, 1 or 2 #M selenite and 0, 1 or 2 uM arsenite. DNA isolated from Caco-2 cells not treated with selenite was significantly (p<0.0001) hypomethylated compared to that from cells treated with 1 or 2 uM selenite. DNA isolated from Caco-2 cells not treated with arsenite was significantly (p<0.0001) hypomethylated compared to DNA isolated from cells treated with 1 or 2 uM arsenite. In addition, methylation of the p53 promoter region of Caco-2 cells decreased when cells were cultured in the absence of selenite and in the absence of arsenite. Similar to the results with Caco-2 cells, rats fed selenium- deficient diets had significantly (p<0.0001) hypomethylated DNA compared to rats fed 0.1 or 2.0 ug selenium/g diets as either selenite or selenomethionine. However, supplemental dietary arsenic (5 ug/g diet) tended (p=0.08) to decrease DNA methylation. Thus, alterations in DNA methylation may be a potential mechanism whereby deficient dietary selenium increases tumorigenesis.