Arriagada, Alejandro A.Albornoz, EduardoOpazo, Ma. CeciliaBecerra, AlvaroVidal, GonzaloFardella, CarlosMichea, LuisCarrasco, NancySimon, FelipeElorza, Alvaro A.Bueno, Susan M.Kalergis, Alexis M.2023-06-222023-06-222015-04Endocrinology (United States). Volume 156, Issue 4, Pages 1540 - 1551. 1 April 20150013-7227https://repositorio.unab.cl/xmlui/handle/ria/50980Indexación: Scopus.This 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.Na+/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.enTiroides-TRH-TSHEndocrinology and DiabetesThyroid GlandSymporter (NIS)Thyroid HormonesArtículoAtribution 4.0 International (CC BY 4.0)10.1210/en.2014-1371