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ARS Home » Plains Area » Grand Forks, North Dakota » Grand Forks Human Nutrition Research Center » Dietary Prevention of Obesity-related Disease Research » Research » Publications at this Location » Publication #219640
Title: High dietary intake of sodium selenite does not affect gene mutation frequency in rat colon and liver

Author
item Zeng, Huawei
item Uthus, Eric
item ROSS, SHARON - NATL CANCER INSTITUTE
item DAVIS, CINDY - NATL CANER INSTITUTE

Submitted to: Journal of Federation of American Societies for Experimental Biology
Publication Type: Abstract Only
Publication Acceptance Date: 2/4/2008
Publication Date: 4/15/2008
Citation: Zeng, H., Uthus, E.O., Ross, S.A., Davis, C.D. 2008. High dietary intake of sodium selenite does not affect gene mutation frequency in rat colon and liver. [abstract] Journal of Federation of American Societies for Experimental Biology. 22:146.7.

Interpretive Summary:

Technical Abstract: Gene mutations have been implicated in the etiology of cancer. In the present study, we utilized Big Blue transgenic rats to evaluate the in vivo mutation frequency of the ' cII gene in rats fed either a Se-deficient (0 µg Se/g diet) or selenium-supplemented diet (2 µg Se/g diet) (n=6 rats/diet) and injected with dimethylhydrazine (DMH) (25 mg/kg body weight, i.p.). There were no differences in body weight (252~264 g) between the Se-deficient and Se-supplemented rats, but liver glutathione peroxidase and thioredoxin reductase activities were significantly lower (p<0.0001) in Se-deficient rats (17.20 and 1.24 U/mg) compared to rats supplemented with Se (607.68 and 4.59 U/mg, respectively). Gene mutation frequency was significantly lower in liver (140~146 mutants per 106 ' cII gene sites) than in colon (579~604 mutants per 106 ' cII gene sites), and there were no differences in gene mutation frequency in DNA from colon mucosa or liver from rats fed the Se-deficient diet compared to those fed the Se-supplemented diet. While previous studies have shown that selenium is protective against DMH-induced preneoplastic colon cancer lesions, the current results suggest that it does not inhibit DMH-induced mutations in the ' cII gene.