Selenoprotein gene expression during selenium-repletion of selenium-deficient rats |
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Authors: | Giovanna Bermano Fergus Nicol John A Dyer Roger A Sunde Geoffrey J Beckett John R Arthur John E Hesketh |
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Institution: | (1) Rowett Research Institute, Bucksburn, AB2 9SB Aberdeen, UK;(2) University of Missouri-Columbia, 65211 Columbia, MO;(3) Cellular Endocrinology Unit, University Department of Clinical Biochemistry, The Royal Infirmary, EH3 9YW Edinburgh, UK |
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Abstract: | Selenium repletion of selenium-deficient rats with 20 μg selenium/kg body weight as Na2SeO3 was used as a model to investigate the mechanisms that control the distribution of the trace element to specific selenoproteins
in liver and thyroid. Cytosolic glutathione peroxidase (cGSHPx), phospholipid hydroperoxide glutathione peroxidase (PHGSHPx),
and iodothyronine 5′-deiodinase (IDI) activities were all transiently increased in liver 16 to 32 h after ip injection with
selenium. However, only cGSHPx and PHGSHPx activities increased in the thyroid where IDI activity was already increased by
selenium deficiency. These responses were owing to synthesis of the seleoproteins on newly synthesised and/or existing mRNAs.
The selenoprotein mRNAs in the thyroid gland were increased two- and threefold after the transitory increases in selenoprotein
activity. In contrast, there were parallel changes in selenoprotein mRNAs and enzyme activities in the liver, with no prolonged
rises in mRNA levels. The organ differences suggest that increased thryotrophin (TSH) concentrations, which are known to induce
thyrodial IDI and mRNA, may control the mRNAs for all the thyroidal selenoproteins investigated and be a major mechanism for
the preservation of thyroidal selenoproteins when selenium supplies are limited. |
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Keywords: | Selenium thyroid deiodinase glutathione peroxidase mRNA gene expression |
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