Excess iodide induces an acute inhibition of the sodium/iodide symporter in thyroid male rat cells by increasing reactive oxygen species
Author
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Arriagada, Alejandro A.
Author
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Albornoz, Eduardo
Author
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Opazo, María Cecilia
Author
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Becerra, Álvaro
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Vidal, Gonzalo
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Fardella, Carlos
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Michea Acevedo, Luis
Author
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Carrasco, Nancy
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Simón, Felipe
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Elorza, Álvaro A.
Author
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Bueno, Susan M.
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Kalergis, Alexis M.
Author
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Riedel, Claudia A.
Admission date
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2015-08-25T02:11:49Z
Available date
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2015-08-25T02:11:49Z
Publication date
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2015
Cita de ítem
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Endocrinology, April 2015, 156(4):1540 –1551
en_US
Identifier
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DOI: 10.1210/en.2014-1371
Identifier
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https://repositorio.uchile.cl/handle/2250/133080
General note
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Artículo de publicación ISI
en_US
Abstract
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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.