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Selenoenzyme expression in thyroid and liver of second generation selenium- and iodine-deficient rats.
J Mol Endocrinol 1996; 16(3):259-67JM

Abstract

The stimulation of thyroid hormone synthesis in iodine deficiency may increase the requirement for the selenoproteins which are involved in thyroid hormone synthesis in the thyroid gland. Selenoenzyme activity and expression were investigated in the thyroid and liver of second generation selenium-and/or iodine-deficient rats. Selenium deficiency caused substantial decreases in hepatic selenium-containing type I iodothyronine deiodinase (ID-I) and cytosolic glutathione peroxidase (cGSHPx) activities and mRNA abundances, but phospholipid hydroperoxide glutathione peroxidase (phGSHPx) activity was only 55% of selenium-supplemented control levels, despite the absence of change in its mRNA abundance. Selenoenzyme mRNA concentrations were maintained at control levels in thyroid glands from the selenium-deficient rat pups. Despite this, a differential effect was observed in selenoenzyme activities: ID-I activity was decreased to 61%, cGSHPx activity to 45% and phGSHPx to 29% of that in selenium-adequate controls. In iodine-deficient thyroid glands, mRNA levels were increased 2.2, 5.0 and 2.8 times for ID-I, cGSHPx and phGSHPx respectively. ID-I and cGSHPx enzyme activities were also increased but the activity of phGSHPx was decreased despite the high mRNA abundance. Thyroid selenoprotein mRNA levels were also increased in combined selenium and iodine deficiency but again there were differential effects on enzyme activities, with ID-I activity increased, cGSHPx unchanged and phGSHPx decreased. Thus, iodine deficiency may produce an oxidant stress on the thyroid gland, increasing the requirement for selenium to maintain selenoenzyme activity. When dietary supplies of selenium are limiting, thyroid selenoprotein mRNA levels are increased to compensate for overall lack of the micronutrient. Furthermore, there is a preferential supply of available selenium to ID-I and cGSHPx to allow maintenance of thyroid function.

Authors+Show Affiliations

Rowett Research Institute, Bucksburn, Aberdeen, UK.No affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

8782084

Citation

Mitchell, J H., et al. "Selenoenzyme Expression in Thyroid and Liver of Second Generation Selenium- and Iodine-deficient Rats." Journal of Molecular Endocrinology, vol. 16, no. 3, 1996, pp. 259-67.
Mitchell JH, Nicol F, Beckett GJ, et al. Selenoenzyme expression in thyroid and liver of second generation selenium- and iodine-deficient rats. J Mol Endocrinol. 1996;16(3):259-67.
Mitchell, J. H., Nicol, F., Beckett, G. J., & Arthur, J. R. (1996). Selenoenzyme expression in thyroid and liver of second generation selenium- and iodine-deficient rats. Journal of Molecular Endocrinology, 16(3), pp. 259-67.
Mitchell JH, et al. Selenoenzyme Expression in Thyroid and Liver of Second Generation Selenium- and Iodine-deficient Rats. J Mol Endocrinol. 1996;16(3):259-67. PubMed PMID: 8782084.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Selenoenzyme expression in thyroid and liver of second generation selenium- and iodine-deficient rats. AU - Mitchell,J H, AU - Nicol,F, AU - Beckett,G J, AU - Arthur,J R, PY - 1996/6/1/pubmed PY - 1996/6/1/medline PY - 1996/6/1/entrez SP - 259 EP - 67 JF - Journal of molecular endocrinology JO - J. Mol. Endocrinol. VL - 16 IS - 3 N2 - The stimulation of thyroid hormone synthesis in iodine deficiency may increase the requirement for the selenoproteins which are involved in thyroid hormone synthesis in the thyroid gland. Selenoenzyme activity and expression were investigated in the thyroid and liver of second generation selenium-and/or iodine-deficient rats. Selenium deficiency caused substantial decreases in hepatic selenium-containing type I iodothyronine deiodinase (ID-I) and cytosolic glutathione peroxidase (cGSHPx) activities and mRNA abundances, but phospholipid hydroperoxide glutathione peroxidase (phGSHPx) activity was only 55% of selenium-supplemented control levels, despite the absence of change in its mRNA abundance. Selenoenzyme mRNA concentrations were maintained at control levels in thyroid glands from the selenium-deficient rat pups. Despite this, a differential effect was observed in selenoenzyme activities: ID-I activity was decreased to 61%, cGSHPx activity to 45% and phGSHPx to 29% of that in selenium-adequate controls. In iodine-deficient thyroid glands, mRNA levels were increased 2.2, 5.0 and 2.8 times for ID-I, cGSHPx and phGSHPx respectively. ID-I and cGSHPx enzyme activities were also increased but the activity of phGSHPx was decreased despite the high mRNA abundance. Thyroid selenoprotein mRNA levels were also increased in combined selenium and iodine deficiency but again there were differential effects on enzyme activities, with ID-I activity increased, cGSHPx unchanged and phGSHPx decreased. Thus, iodine deficiency may produce an oxidant stress on the thyroid gland, increasing the requirement for selenium to maintain selenoenzyme activity. When dietary supplies of selenium are limiting, thyroid selenoprotein mRNA levels are increased to compensate for overall lack of the micronutrient. Furthermore, there is a preferential supply of available selenium to ID-I and cGSHPx to allow maintenance of thyroid function. SN - 0952-5041 UR - https://www.unboundmedicine.com/medline/citation/8782084/Selenoenzyme_expression_in_thyroid_and_liver_of_second_generation_selenium__and_iodine_deficient_rats_ DB - PRIME DP - Unbound Medicine ER -