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Thyroid stimulating hormone and selenium supply interact to regulate selenoenzyme gene expression in thyroid cells (FRTL‐5) in culture
Author(s) -
Villette Stéphane,
Bermano Giovanna,
Arthur John R.,
Hesketh John E.
Publication year - 1998
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(98)01280-0
Subject(s) - deiodinase , medicine , endocrinology , hormone , glutathione peroxidase , selenium , thyroid , thyroid peroxidase , chemistry , iodothyronine deiodinase , peroxidase , selenocysteine , thyroid stimulating hormone , enzyme , glutathione , biology , biochemistry , triiodothyronine , organic chemistry , cysteine
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.