Abstract
In the absence of a sodium selenite supplement, FRTL-5 cells showed a reduced activity of cytosolic glutathione peroxidase (cGSH-Px), a marker of selenium status, indicating the cells were Se-deficient. Se-deficient cells showed a 65% reduction in cGSH-Px mRNA abundance but little change in abundance of either phospholipid hydroperoxide glutathione peroxidase or type 1 deiodinase (IDI) mRNA. In Se-replete cells increased thyroid stimulating hormone (TSH) caused a small decrease in IDI abundance but in Se-deficient cells TSH caused a large increase. The results indicate an interaction between TSH and Se status in the regulation of thyroid selenoenzyme synthesis.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Blotting, Northern
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Cell Line
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Culture Media
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Cytosol / enzymology
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Epithelial Cells / metabolism
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Gene Expression Regulation, Enzymologic*
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Glutathione Peroxidase / genetics*
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Glutathione Peroxidase / metabolism
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Humans
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Iodide Peroxidase / genetics
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Phospholipid Hydroperoxide Glutathione Peroxidase
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RNA, Messenger / analysis
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Rats
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Selenium / deficiency
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Selenium / metabolism
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Selenium / pharmacology*
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Thyroid Gland / cytology
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Thyroid Gland / enzymology*
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Thyrotropin / pharmacology*
Substances
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Culture Media
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RNA, Messenger
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Thyrotropin
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Phospholipid Hydroperoxide Glutathione Peroxidase
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Iodide Peroxidase
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Glutathione Peroxidase
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Selenium