par Corvilain, Bernard 
;Contempre, Bernard ;Longombé, Ahuka O.;Goyens, Philippe ;Gervy Decoster, Christine ;Lamy, Françoise ;Vanderpas, Jean-Baptiste ;Dumont, Jacques Emile
Référence The American journal of clinical nutrition, 57, 2 Suppl, page (244-248)
Publication Publié, 1993-02
;Contempre, Bernard ;Longombé, Ahuka O.;Goyens, Philippe ;Gervy Decoster, Christine ;Lamy, Françoise ;Vanderpas, Jean-Baptiste ;Dumont, Jacques Emile Référence The American journal of clinical nutrition, 57, 2 Suppl, page (244-248)
Publication Publié, 1993-02
Article révisé par les pairs
| Résumé : | 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. |
