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Selenium‐regulated expression of non‐selenoprotein genes
Author(s) -
Raines Anna M.,
Sunde Roger A.
Publication year - 2009
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.23.1_supplement.346.4
Subject(s) - selenoprotein , selenoprotein p , gene , biology , biomarker , candidate gene , gene expression , selenium , downregulation and upregulation , gene expression profiling , selenium deficiency , dna microarray , endocrinology , medicine , genetics , chemistry , oxidative stress , glutathione peroxidase , superoxide dismutase , organic chemistry
Recent studies have linked super‐nutritional Se intake to both beneficial and adverse outcomes such as lowered risk for cancer and increased risk for type II diabetes. These paradoxical effects of high Se intake highlight the need for biomarkers of high Se status. While a subset of selenoprotein mRNAs are useful as biomarkers of Se deficiency, no selenoprotein mRNAs further increase at super‐nutritional intakes, precluding their use as biomarkers of high Se. To identify non‐selenoprotein genes regulated by Se, we used microarrays to analyze gene expression in liver and kidney from mice fed < 0.007 (‐Se), 0.05 (~Se), or 0.2 μg Se/g diet (+Se). Comparison analysis of expression in +Se vs. ~Se and +Se vs. ‐Se yielded 103 unique candidate biomarker genes changed = 1.4 fold. Detected selenoproteins show the expected pattern of Se‐regulation. The Se‐dependent expression of non‐selenoprotein genes is being confirmed by qRT‐PCR and tested in rats fed 0‐0.8 μg Se/g diet. So far, we have identified 6 genes changed > 3 fold only in +Se, and 1 transporter gene upregulated only in ‐Se in both mice and rats. Interestingly, four distinct patterns of Se‐regulation have emerged among the candidates: high in +Se; low in +Se; high in ‐Se; low in ‐Se (selenoprotein pattern). Candidate genes may be useful as high Se biomarkers and could be involved in Se homeostasis in Se deficiency or Se excess. Support: DK74184, DK07665, WISC04909 Grant Funding Source NIH