Cytochrome P450 Catalyzed Covalent Binding of Methoxychlor to Rat Hepatic, Microsomal Iodothyronine 5′-Monodeiodinase, Type I: Does Exposure to Methoxychlor Disrupt Thyroid Hormone Metabolism?

1995 ◽  
Vol 322 (2) ◽  
pp. 390-394 ◽  
Author(s):  
L.X. Zhou ◽  
S.S. Dehal ◽  
D. Kupfer ◽  
S. Morrell ◽  
B.A. Mckenzie ◽  
...  
Keyword(s):  
Cytochrome P450 ◽  
Thyroid Hormone ◽  
Covalent Binding ◽  
Type I ◽  
Hormone Metabolism ◽  
Thyroid Hormone Metabolism

The role of selenium in thyroid hormone metabolism

1991 ◽  
Vol 69 (11) ◽  
pp. 1648-1652 ◽  
Author(s):  
John R. Arthur
Keyword(s):  
Thyroid Hormone ◽  
Iodine Deficiency ◽  
Selenium Deficiency ◽  
Major Influence ◽  
Type I ◽  
Hormone Metabolism ◽  
Thyroid Hormone Metabolism ◽  
Iodothyronine Deiodinases ◽  
Clinical Changes

In animals, decreases in selenium-containing glutathione peroxidase activity and the resultant impairment of peroxide metabolism can account for many, but not all of the biochemical and clinical changes caused by selenium deficiency. Recently, however, type I iodothyronine 5′-deiodinase has also been shown to be a selenium-containing enzyme. This explains the impairment of thyroid hormone metabolism caused by selenium deficiency in animals with a normal vitamin E status. Since iodothyronine 5′-deiodinases are essential for the production of the active thyroid hormone 3,5,3′-triiodothyronine, some of the consequences of selenium deficiency may result from thyroid changes rather than inability to metabolise peroxides. In particular, the impaired thyroid hormone metabolism may be responsible for decreased growth and resistance to cold stress in selenium-deficient animals. A further consequence of the role of selenium in thyroid hormone metabolism is the exacerbation of some of the thyroid changes in iodine deficiency by a concurrent selenium deficiency. Selenium status may therefore have a major influence on the outcome of iodine deficiency in both human and animal populations.Key words: selenium, thyroid hormones, iodothyronine deiodinases, iodine, nutritional disorders.

scholarly journals Effects of concomitant selenium and vitamin E administration on thyroid hormone metabolism in broilers

2018 ◽  
Vol 68 (3) ◽  
pp. 355
Author(s):  
A. C. PAPPAS ◽  
B. M. KOTSAMPASI ◽  
K. KALAMARAS ◽  
K. FEGEROS ◽  
G. ZERVAS ◽  
...  
Keyword(s):  
Vitamin E ◽  
Thyroid Hormone ◽  
Control Diet ◽  
Dietary Treatment ◽  
Tocopheryl Acetate ◽  
Type I ◽  
Hormone Metabolism ◽  
Iodothyronine Deiodinase ◽  
Thyroid Hormone Metabolism ◽  
Diet Control

A total of 400, as hatched, broilers were used to investigate the effect of selenium (Se) and vitamin E supplementation on thyroid hormones metabolism. There were 5 replicates of 4 dietary treatments namely: control (C), a soybean meal maize basal diet with adequate Se and vitamin E (0.3 mg Se per kg diet and 80 mg vitamin E per kg diet), control diet with Se added (Se+, with an additional 1 mg of Se per kg of diet), control diet with vitamin E added (E+, with an additional 350 mg of vitamin E per kg of diet) and Se+E+ (with additional 1 mg of Se and 350 mg of vitamin E per kg of diet). Diets were isonitrogenous and isocaloric. Zinc L-selenomethionine complex was used to increase Se content and dl-α-tocopheryl acetate to increase vitamin E content. The experiment lasted 42 days. Plasma Se concentration increased in Se+ groups, while whole blood glutathione peroxidase (GPx) activity increased in Se+, E+ and Se+E+ groups compared to control. Hepatic type I iodothyronine deiodinase (ID-I) and thyroid hormone concentrations were unaffected by any dietary treatment. It is concluded that supplementation with Se or vitamin Ε alone or in combination above animal’s requirements does not affect thyroid hormone metabolism and liver ID-I activity under the conditions examined.

Effect of Interleukin-1 (IL-1) on Thyroid Hormone Metabolism in Mice: Stimulation by IL-1 of Iodothyronine 5′-Deiodinating Activity (Type I) in the Liver*

Endocrinology ◽  
1989 ◽  
Vol 124 (1) ◽  
pp. 167-174 ◽  
Author(s):  
TORU FUJII ◽  
KANJI SATO ◽  
MINORU OZAWA ◽  
KEIZO KASONO ◽  
HIDEHITO IMAMURA ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Interleukin 1 ◽  
Type I ◽  
Activity Type ◽  
Hormone Metabolism ◽  
Thyroid Hormone Metabolism

scholarly journals Changes in myocardial thyroid hormone metabolism and α-glycerophosphate dehydrogenase activity in rats deficient in iodine and selenium

1997 ◽  
Vol 78 (4) ◽  
pp. 671-676 ◽  
Author(s):  
H. Y. Wu ◽  
Y. M. Xia ◽  
P. C. Ha ◽  
X. S. Chen
Keyword(s):  
Thyroid Hormone ◽  
Glutathione Peroxidase ◽  
Peroxidase Activity ◽  
Keshan Disease ◽  
Type I ◽  
Glutathione Peroxidase Activity ◽  
Hormone Metabolism ◽  
Thyroid Hormone Metabolism ◽  
Glycerophosphate Dehydrogenase ◽  
Plasma Triiodothyronine

Weanling Wistar rats were fed on diets prepared from grain from areas deficient in I and Se where Keshan disease is endemic. Rats were divided into four groups, each of twelve rats, and received a diet supplemented with: I, Se, I + Se or nothing. At 8 weeks after weaning, myocardial α-glycerophosphate dehydrogenase (EC 1.1.1.8; α-GPD) activity and indices of Se and thyroid hormone status were determined. The group supplemented with iodine had increased plasma thyroxine levels. There was no difference in plasma triiodothyronine concentration between the groups but triiodothyronine levels in heart were reduced in the Se-supplemented group. Se supplementation increased myocardial glutathione peroxidase activity (EC 1.11.1.9) and the type I 5'-deiodinase (EC 3.8.1.4) activity in rat liver, but no type I 5'-deiodinase activity was detected in heart. α-GDP activity in heart was increased in the group supplemented with Se, I or both. There was a significant relationship (P < 0.05) between myocardial α-GDP activity and plasma thyroxine levels but not between α-GDP and myocardial glutathione peroxidase activity. The results indicate that iodine may be more important than Se in energy metabolism in the myocardium, which may give a new insight for the study of the aetiology of Keshan disease in areas where foodstuffs are deficient in both Se and I.

Effects of energy restriction on thyroid hormone metabolism in chickens

2009 ◽  
Vol 57 (2) ◽  
pp. 319-330 ◽  
Author(s):  
Andrea Győrffy ◽  
Ahmed Sayed-Ahmed ◽  
Attila Zsarnovszky ◽  
Vilmos Frenyó ◽  
Eddy Decuypere ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Energy Restriction ◽  
Feed Restriction ◽  
Type I ◽  
Activity Levels ◽  
Serum Concentrations ◽  
Hormone Metabolism ◽  
Adaptation Mechanism ◽  
Thyroid Hormone Metabolism

Energy restriction induces changes in thyroid hormone economy in the form of a complex adaptation mechanism, in order to conserve energy storage and protein reserves. In the present work, thyroid hormone serum concentrations, hepatic deiodinase enzyme activities and hepatic deiodinase mRNA expression were examined after feed restriction and fasting. We demonstrate that during energy restriction, T 3 concentration is lowered due to a decreased T 4 activation and increased T 3 inactivation. We show that hepatic type-I deiodinase (D1) is not affected by energy restriction, however, hepatic D2 is decreased on both transcriptional and enzyme activity levels. Furthermore, hepatic D3 is increased after feed restriction in the liver. We also show that the hypothalamic feedback is not involved in the changes in serum T 3 and T 4 concentrations. Our data indicate that D2 enzyme contributes to the special hormone-exporting role of the chicken liver and this enzyme can be modulated by feed restriction.

scholarly journals Developmentally defined regulation of thyroid hormone metabolism by glucocorticoids in the rat

2005 ◽  
Vol 185 (2) ◽  
pp. 327-336 ◽  
Author(s):  
S Van der Geyten ◽  
V M Darras
Keyword(s):  
Thyroid Hormone ◽  
Direct Consequence ◽  
Type I ◽  
Hormone Metabolism ◽  
Hormone Levels ◽  
Thyroid Hormone Metabolism ◽  
Rat Pups ◽  
Short Period ◽  
Thyroid Hormone Levels

Glucocorticoids are known regulators of thyroid function in vertebrates. In birds they have clear tissue-specific and age-dependent effects on thyroid hormone metabolism. In mammals, however, few studies exist addressing these aspects using an in vivo model system. We therefore set out to examine the acute effects of a single dose of dexamethasone (DEX) on plasma 3,5,3′-tri-iodothyronine (T3) and thyroxine (T4) levels, as well as on the activity of the different deiodinases in liver, kidney and brain in the developing rat. In 20-day-old fetuses (E20), glucocorticoids had no effects on circulating thyroid hormone levels despite their clear effects on hepatic and renal deiodinases, thereby indicating that under these conditions circulating thyroid hormone levels are more dependent on thyroidal secretion than on peripheral deiodination. In contrast, in 5-day-old rat pups, DEX did not seem to have any effects on hepatic and renal T3 production (via the type I deiodinase), whereas type III deiodinase (D3) activity in both these tissues increased significantly. These observations therefore suggested that the DEX-induced increase in circulating T3 levels is a direct consequence of the increase in plasma T4 levels. In 12-day-old pups (P12), however, the main effect of glucocorticoids on circulating levels was by increasing inner ring deiodination T3 through induction of D3 in both liver and kidney. Finally, in the brain, glucocorticoids stimulated thyroid hormone activity only during a short period of time (between E20 and P12) that largely overlaps with the transient window in time during which brain development is thyroid hormone sensitive. This was in contrast to the E20 and P12 brain, where the glucocorticoid-induced changes in type II deiodinase and D3 seemed to favor a status quo in local T3 availability.

scholarly journals Type 1 iodothyronine deiodinase in human physiology and disease

2011 ◽  
Vol 209 (3) ◽  
pp. 283-297 ◽  
Author(s):  
Ana Luiza Maia ◽  
Iuri Martin Goemann ◽  
Erika L Souza Meyer ◽  
Simone Magagnin Wajner
Keyword(s):  
Human Physiology ◽  
Thyroid Hormone ◽  
Active Form ◽  
Normal Function ◽  
Type I ◽  
Hormone Metabolism ◽  
Iodothyronine Deiodinase ◽  
Thyroid Hormone Metabolism ◽  
Iodothyronine Deiodinases

Thyroid hormone is essential for the normal function of virtually all tissues. The iodothyronine deiodinases catalyze the removal of an iodine residue from the pro-hormone thyroxine (T4) molecule, thus producing either the active form triiodothyronine (T3; activation) or inactive metabolites (reverse T3; inactivation). Type I deiodinase (D1) catalyzes both reactions. Over the last years, several studies have attempted to understand the mechanisms of D1 function, underlying its effects on normal thyroid hormone metabolism and pathological processes. Although peripheral D1-generated T3 production contributes to a portion of plasma T3 in euthyroid state, pathologically increased thyroidal D1 activity seems to be the main cause of the elevated T3 concentrations observed in hyperthyroid patients. On the other hand, D1-deficient mouse models show that, in the absence of D1, inactive and lesser iodothyronines are excreted in feces with the loss of associated iodine, demonstrating the scavenging function for D1 that might be particularly important in an iodine deficiency setting. Polymorphisms in the DIO1 gene have been associated with changes in serum thyroid hormone levels, whereas decreased D1 activity has been reported in the nonthyroid illness syndrome and in several human neoplasias. The current review aims at presenting an updated picture of the recent advances made in the biochemical and molecular properties of D1 as well as its role in human physiology.

scholarly journals Inhibition of type I and type II iodothyronine deiodinase activity in rat liver, kidney and brain produced by selenium deficiency

1989 ◽  
Vol 259 (3) ◽  
pp. 887-892 ◽  
Author(s):  
G J Beckett ◽  
D A MacDougall ◽  
F Nicol ◽  
J R Arthur
Keyword(s):  
Body Weight ◽  
Thyroid Hormone ◽  
Feedback Inhibition ◽  
Selenium Deficiency ◽  
Stress Factors ◽  
Type I ◽  
Type Ii ◽  
Hormone Metabolism ◽  
Iodothyronine Deiodinase ◽  
Thyroid Hormone Metabolism

Selenium deficiency for periods of 5 or 6 weeks in rats produced an inhibition of tri-iodothyronine (T3) production from added thyroxine (T4) in brain, liver and kidney homogenate. This inhibition was reflected in plasma T4 and T3 concentrations, which were respectively increased and decreased in selenium-deficient animals. Although plasma T4 levels increased in selenium-deficient animals, this did not produce the normal feedback inhibition on thyrotropin release from the pituitary. Selenium deficiency was confirmed in the animals by decreased selenium-dependent glutathione peroxidase (Se-GSH-Px) activity in all of these tissues. Administration of selenium, as a single intraperitoneal injection of 200 micrograms of selenium (as Na2SeO3)/kg body weight completely reversed the effects of selenium deficiency on thyroid-hormone metabolism and partly restored the activity of Se-GSH-Px. Selenium administration at 10 micrograms/kg body weight had no significant effect on thyroid-hormone metabolism or on Se-GSH-Px activity in any of the tissues studied. The characteristic changes in plasma thyroid-hormone levels that occurred in selenium deficiency appeared not to be due to non-specific stress factors, since food restriction to 75% of normal intake or vitamin E deficiency produced no significant changes in plasma T4 or T3 concentration. These data are consistent with the view that the Type I and Type II iodothyronine deiodinase enzymes are seleno-enzymes or require selenium-containing cofactors for activity.

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