Excess iodide induces an acute inhibition of the sodium/iodide symporter in thyroid male rat cells by increasing reactive oxygen species

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dc.contributor.authorArriagada, Alejandro A.
dc.contributor.authorAlbornoz, Eduardo
dc.contributor.authorOpazo, Ma. Cecilia
dc.contributor.authorBecerra, Alvaro
dc.contributor.authorVidal, Gonzalo
dc.contributor.authorFardella, Carlos
dc.contributor.authorMichea, Luis
dc.contributor.authorCarrasco, Nancy
dc.contributor.authorSimon, Felipe
dc.contributor.authorElorza, Alvaro A.
dc.contributor.authorBueno, Susan M.
dc.contributor.authorKalergis, Alexis M.
dc.date.accessioned2023-06-22T19:36:34Z
dc.date.available2023-06-22T19:36:34Z
dc.date.issued2015-04
dc.descriptionIndexación: Scopus.es
dc.descriptionThis work was supported by Proyecto de Inicio Grant UNAB DI 06-08, Fondecyt Grant 1130996, Fondecyt Grant 1121078, Millennium Institute on Immunology and Immunotherapy Grant P09/016-F, Proyecto Cochilco-Fondecyt 1100995, and Proyecto Núcleo Grant UNAB DI-209-12/N. Disclosure Summary: The authors have nothing to disclose.
dc.description.abstractNa+/I− symporter (NIS) mediates iodide (I−) uptake in the thyroid gland, the first and rate-limiting step in the biosynthesis of the thyroid hormones. The expression and function of NIS in thyroid cells is mainly regulated by TSH and by the intracellular concentration of I−. High doses of I− for 1 or 2 days inhibit the synthesis of thyroid hormones, a process known as the Wolff-Chaikoff effect. The cellular mechanisms responsible for this physiological response are mediated in part by the inhibition of I− uptake through a reduction of NIS expression. Here we show that inhibition of I− uptake occurs as early as 2 hours or 5 hours after exposure to excess I− in FRTL-5 cells and the rat thyroid gland, respectively. Inhibition of I− uptake was not due to reduced NIS expression or altered localization in thyroid cells. We observed that incubation of FRTL-5 cells with excess I− for 2 hours increased H2O2 generation. Furthermore, the inhibitory effect of excess I− on NIS-mediated I− transport could be recapitulated by H2O2 and reverted by reactive derived oxygen species scavengers. The data shown here support the notion that excess I− inhibits NIS at the cell surface at early times by means of a posttranslational mechanism that involves reactive derived oxygen species.es
dc.description.urihttps://academic.oup.com/endo/article/156/4/1540/2803807?login=true
dc.identifier.citationEndocrinology (United States). Volume 156, Issue 4, Pages 1540 - 1551. 1 April 2015es
dc.identifier.doi10.1210/en.2014-1371
dc.identifier.issn0013-7227
dc.identifier.urihttps://repositorio.unab.cl/xmlui/handle/ria/50980
dc.language.isoenes
dc.publisherEndocrine Societyes
dc.rights.licenseAtribution 4.0 International (CC BY 4.0)
dc.rights.urihttps://creativecommons.org/licenses/by/4.0/deed.es
dc.subjectTiroides-TRH-TSHes
dc.subjectEndocrinology and Diabeteses
dc.subjectThyroid Gland
dc.subjectSymporter (NIS)
dc.subjectThyroid Hormones
dc.titleExcess iodide induces an acute inhibition of the sodium/iodide symporter in thyroid male rat cells by increasing reactive oxygen specieses
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