AJCN North Carolina Research Campus
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


This Article
Right arrow Full Text (PDF)
Right arrow Purchase Article
Right arrow View Shopping Cart
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Corvilain, B.
Right arrow Articles by Dumont, J. E.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Corvilain, B.
Right arrow Articles by Dumont, J. E.
Agricola
Right arrow Articles by Corvilain, B.
Right arrow Articles by Dumont, J. E.

American Journal of Clinical Nutrition, Vol 57, 244S-248S, Copyright © 1993 by The American Society for Clinical Nutrition, Inc


REVIEW ARTICLES

Selenium and the thyroid: how the relationship was established

B Corvilain, B Contempre, AO Longombe, P Goyens, C Gervy-Decoster, F Lamy, JB Vanderpas and JE Dumont
Department of Pediatrics, School of Public Health, University of Brussels, Belgium.

Several hypotheses concerning consequences of selenium deficiency on iodine metabolism can be proposed on the basis of experimental studies in rats and from epidemiological and experimental studies in humans. By decreasing intracellular GSH peroxidase activity, selenium deficiency may increase hydrogen peroxide (H2O2) supply and lead over several weeks to the thyroid atrophy observed in myxoedematous cretins. By improving thyroid hormone synthesis and by decreasing peripheral thyroxin (T4) deiodination, selenium deficiency could protect fetal brain T4 supply and thus prevent neurologic cretinism. Selenium deficiency may protect against iodine deficiency by decreasing T4 metabolism--and thus iodide leakage and--perhaps also by increasing H2O2 supply and thyroid hormone synthesis and thus thyroid efficiency.


This article has been cited by other articles:


Home page
J EndocrinolHome page
G. J Beckett and J. R Arthur
Selenium and endocrine systems
J. Endocrinol., March 1, 2005; 184(3): 455 - 465.
[Abstract] [Full Text] [PDF]


Home page
Am. J. Physiol. Endocrinol. Metab.Home page
B. Corvilain, L. Collyn, J. van Sande, and J. E. Dumont
Stimulation by iodide of H2O2 generation in thyroid slices from several species
Am J Physiol Endocrinol Metab, April 1, 2000; 278(4): E692 - E699.
[Abstract] [Full Text] [PDF]


Home page
NEJMHome page
R. D. Utiger
Kashin-Beck Disease -- Expanding the Spectrum of Iodine-Deficiency Disorders
N. Engl. J. Med., October 15, 1998; 339(16): 1156 - 1158.
[Full Text]


Home page
J. Nutr.Home page
C. S. Hotz, D. W. Fitzpatrick, K. D. Trick, and M. R. L'Abbé
Dietary Iodine and Selenium Interact To Affect Thyroid Hormone Metabolism of Rats
J. Nutr., June 1, 1997; 127(6): 1214 - 1218.
[Abstract] [Full Text]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 1993 by The American Society for Nutrition