title: Selenium and iodine deficiencies: effects on brain and brown adipose tissue selenoenzyme activity and expression.
abstract: Adequate dietary iodine supplies and thyroid hormones are needed for the development of the central nervous system (CNS) and brown adipose tissue (BAT) function. Decreases in plasma thyroxine (T4) concentrations may increase the requirement for the selenoenzymes types I and II iodothyronine deiodinase (ID-I and ID-II) in the brain and ID-II in BAT to protect against any fall in intracellular 3,3',5 tri-iodothyronine (T3) concentrations in these organs. We have therefore investigated selenoenzyme activity and expression and some developmental markers in brain and BAT of second generation selenium- and iodine-deficient rats. Despite substantial alterations in plasma thyroid hormone concentrations and thyroidal and hepatic selenoprotein expression in selenium and iodine deficiencies, ID-I, cytosolic glutathione peroxidase (cGSHPx) and phospholipid hydroperoxide glutathione peroxidase (phGSHPx) activities and expression remained relatively constant in most brain regions studied. Additionally, brain and pituitary ID-II activities were increased in iodine deficiency regardless of selenium status. This can help maintain tissue T3 concentrations in hypothyroidism. Consistent with this, no significant effects of iodine or selenium deficiency on the development of the brain were observed, as assessed by the activities of marker enzymes. In contrast, BAT from selenium- and iodine deficient rats had impaired thyroid hormone metabolism and less uncoupling protein than in tissue from selenium- and iodine-supplemented animals. Thus, the effects of selenium and iodine deficiency on the brain are limited due to the activation of the compensatory mechanisms but these mechanisms are less effective in BAT.
authors.affiliation: Rowett Research Institute, Bucksburn, Aberdeen, UK.
authors.forename: J H
authors.initials: JH
authors.lastname: Mitchell
authors.forename: F
authors.initials: F
authors.lastname: Nicol
authors.forename: G J
authors.initials: GJ
authors.lastname: Beckett
authors.forename: J R
authors.initials: JR
authors.lastname: Arthur
mesh_terms: D002001:Adipose Tissue, Brown / Q000201:enzymology*; D000818:Animals; D001921:Brain / Q000201:enzymology* / Q000254:growth & development; D003600:Cytosol / Q000201:enzymology; D004789:Enzyme Activation; D005979:Glutathione Peroxidase / Q000235:genetics / Q000378:metabolism; D017403:In Situ Hybridization; D007453:Iodide Peroxidase / Q000235:genetics / Q000378:metabolism*; D007455:Iodine / Q000172:deficiency*; D000080662:Phospholipid Hydroperoxide Glutathione Peroxidase; D012333:RNA, Messenger / Q000032:analysis; D051381:Rats; D012643:Selenium / Q000172:deficiency*; D013963:Thyroid Hormones / Q000378:metabolism
chemical_list: D012333:RNA, Messenger; D013963:Thyroid Hormones; D007455:Iodine; D000080662:Phospholipid Hydroperoxide Glutathione Peroxidase; D007453:Iodide Peroxidase; D005979:Glutathione Peroxidase; D012643:Selenium