Selenoprotein expression and brain development in preweanling selenium- and iodine-deficient rats

J H Mitchell, Fergus Nicol, G J Beckett, John Arthur

Research output: Contribution to journalArticle

44 Citations (Scopus)

Abstract

Selenium deficiency causes further impairment of thyroid hormone metabolism in iodine-deficient rats and therefore could have a role in the aetiology of both myxoedematous and neurological cretinism in humans. Thyroidal type I iodothyronine deiodinase (ID-I), cytosolic glutathione peroxidase and phospholipid hydroperoxide glutathione peroxidase activities were increased in iodine-deficient adult rats and their offspring at 11 days of age. Thyroidal ID-I activity was unchanged and thyroidal cytosolic glutathione peroxidase activity was decreased by more than 75% by combined selenium and iodine deficiency in 11-day-old rats, indicating that, while the thyroid retained an ability to produce 3,3',5-triiodothyronine (T-3), the gland was probably more susceptible to peroxidative damage caused by increased hydrogen peroxide concentrations driven by increased thyrotrophin. Thyroidal atrophy, common in myxoedematous cretinism, did not occur in iodine-or selenium and iodine-deficient rat pups. Iodine deficiency increased brain type II iodothyronine deiodinase activity 1.5-fold in 4-day-old rats and 3-fold in 11-day-old rats, regardless of selenium status. Thus rats were able to activate compensatory mechanisms in brain that would maintain T-3 concentrations in selenium and iodine deficiencies. Surprisingly, however, selenium deficiency had a greater effect than iodine deficiency on markers of brain development in rat pups. Expression of the brain-derived neurotrophic factor (BDNF) nRNA was decreased in selenium deficiency in 4- and 11-day-old pups and in combined selenium and iodine deficiency in 4-day-old pups. Iodine deficiency caused an increase in BDNF expression in 11-day-old pups but had no effect on 4-day-old pups. Myelin basic protein mRNA expression in brain was decreased by combined selenium and iodine deficiency in 11-day-old rats.

Original languageEnglish
Pages (from-to)203-210
Number of pages8
JournalJournal of Molecular Endocrinology
Volume20
Issue number2
Publication statusPublished - Apr 1998

Keywords

  • THYROID-HORMONES
  • SUPPLEMENTATION
  • 5'-DEIODINASE
  • CLONING
  • GENE
  • RNA

Cite this

Selenoprotein expression and brain development in preweanling selenium- and iodine-deficient rats. / Mitchell, J H ; Nicol, Fergus; Beckett, G J ; Arthur, John.

In: Journal of Molecular Endocrinology, Vol. 20, No. 2, 04.1998, p. 203-210.

Research output: Contribution to journalArticle

Mitchell, JH, Nicol, F, Beckett, GJ & Arthur, J 1998, 'Selenoprotein expression and brain development in preweanling selenium- and iodine-deficient rats', Journal of Molecular Endocrinology, vol. 20, no. 2, pp. 203-210.
Mitchell, J H ; Nicol, Fergus ; Beckett, G J ; Arthur, John. / Selenoprotein expression and brain development in preweanling selenium- and iodine-deficient rats. In: Journal of Molecular Endocrinology. 1998 ; Vol. 20, No. 2. pp. 203-210.
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AB - Selenium deficiency causes further impairment of thyroid hormone metabolism in iodine-deficient rats and therefore could have a role in the aetiology of both myxoedematous and neurological cretinism in humans. Thyroidal type I iodothyronine deiodinase (ID-I), cytosolic glutathione peroxidase and phospholipid hydroperoxide glutathione peroxidase activities were increased in iodine-deficient adult rats and their offspring at 11 days of age. Thyroidal ID-I activity was unchanged and thyroidal cytosolic glutathione peroxidase activity was decreased by more than 75% by combined selenium and iodine deficiency in 11-day-old rats, indicating that, while the thyroid retained an ability to produce 3,3',5-triiodothyronine (T-3), the gland was probably more susceptible to peroxidative damage caused by increased hydrogen peroxide concentrations driven by increased thyrotrophin. Thyroidal atrophy, common in myxoedematous cretinism, did not occur in iodine-or selenium and iodine-deficient rat pups. Iodine deficiency increased brain type II iodothyronine deiodinase activity 1.5-fold in 4-day-old rats and 3-fold in 11-day-old rats, regardless of selenium status. Thus rats were able to activate compensatory mechanisms in brain that would maintain T-3 concentrations in selenium and iodine deficiencies. Surprisingly, however, selenium deficiency had a greater effect than iodine deficiency on markers of brain development in rat pups. Expression of the brain-derived neurotrophic factor (BDNF) nRNA was decreased in selenium deficiency in 4- and 11-day-old pups and in combined selenium and iodine deficiency in 4-day-old pups. Iodine deficiency caused an increase in BDNF expression in 11-day-old pups but had no effect on 4-day-old pups. Myelin basic protein mRNA expression in brain was decreased by combined selenium and iodine deficiency in 11-day-old rats.

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