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High dietary intake of sodium selenite does not affect gene mutation frequency in rat colon and liver
Author(s) -
Zeng Huawei,
Uthus Eric O,
Ross Sharon A,
Davis Cindy D
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.146.7
Subject(s) - medicine , endocrinology , glutathione peroxidase , 1,2 dimethylhydrazine , selenium , mutant , mutation , gene mutation , gene , thioredoxin reductase , thioredoxin , biology , chemistry , azoxymethane , oxidative stress , colorectal cancer , biochemistry , cancer , catalase , organic chemistry
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 λ 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 10 6 λ cII gene sites) than in colon (579∼604 mutants per 10 6 λ 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 λ cII gene.