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

Alejandro A. Arriagada, Eduardo Albornoz, Ma Cecilia Opazo, Alvaro Becerra, Gonzalo Vidal, Carlos Fardella, Luis Michea, Nancy Carrasco, Felipe Simon, Alvaro A. Elorza, Susan M. Bueno, Alexis M. Kalergis, Claudia A. Riedel

Resultado de la investigación: Article

13 Citas (Scopus)

Resumen

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.

Idioma originalEnglish
Páginas (desde-hasta)1540-1551
Número de páginas12
PublicaciónEndocrinology
Volumen156
N.º4
DOI
EstadoPublished - 1 abr 2015

Huella dactilar

Symporters
Iodides
Reactive Oxygen Species
Thyroid Gland
Thyroid Hormones
sodium-iodide symporter

ASJC Scopus subject areas

  • Endocrinology
  • Medicine(all)

Citar esto

Arriagada, Alejandro A. ; Albornoz, Eduardo ; Opazo, Ma Cecilia ; Becerra, Alvaro ; Vidal, Gonzalo ; Fardella, Carlos ; Michea, Luis ; Carrasco, Nancy ; Simon, Felipe ; Elorza, Alvaro A. ; Bueno, Susan M. ; Kalergis, Alexis M. ; Riedel, Claudia A. / Excess iodide induces an acute inhibition of the sodium/iodide symporter in thyroid male rat cells by increasing reactive oxygen species. En: Endocrinology. 2015 ; Vol. 156, N.º 4. pp. 1540-1551.
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title = "Excess iodide induces an acute inhibition of the sodium/iodide symporter in thyroid male rat cells by increasing reactive oxygen species",
abstract = "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.",
author = "Arriagada, {Alejandro A.} and Eduardo Albornoz and Opazo, {Ma Cecilia} and Alvaro Becerra and Gonzalo Vidal and Carlos Fardella and Luis Michea and Nancy Carrasco and Felipe Simon and Elorza, {Alvaro A.} and Bueno, {Susan M.} and Kalergis, {Alexis M.} and Riedel, {Claudia A.}",
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Arriagada, AA, Albornoz, E, Opazo, MC, Becerra, A, Vidal, G, Fardella, C, Michea, L, Carrasco, N, Simon, F, Elorza, AA, Bueno, SM, Kalergis, AM & Riedel, CA 2015, 'Excess iodide induces an acute inhibition of the sodium/iodide symporter in thyroid male rat cells by increasing reactive oxygen species', Endocrinology, vol. 156, n.º 4, pp. 1540-1551. https://doi.org/10.1210/en.2014-1371

Excess iodide induces an acute inhibition of the sodium/iodide symporter in thyroid male rat cells by increasing reactive oxygen species. / Arriagada, Alejandro A.; Albornoz, Eduardo; Opazo, Ma Cecilia; Becerra, Alvaro; Vidal, Gonzalo; Fardella, Carlos; Michea, Luis; Carrasco, Nancy; Simon, Felipe; Elorza, Alvaro A.; Bueno, Susan M.; Kalergis, Alexis M.; Riedel, Claudia A.

En: Endocrinology, Vol. 156, N.º 4, 01.04.2015, p. 1540-1551.

Resultado de la investigación: Article

TY - JOUR

T1 - Excess iodide induces an acute inhibition of the sodium/iodide symporter in thyroid male rat cells by increasing reactive oxygen species

AU - Arriagada, Alejandro A.

AU - Albornoz, Eduardo

AU - Opazo, Ma Cecilia

AU - Becerra, Alvaro

AU - Vidal, Gonzalo

AU - Fardella, Carlos

AU - Michea, Luis

AU - Carrasco, Nancy

AU - Simon, Felipe

AU - Elorza, Alvaro A.

AU - Bueno, Susan M.

AU - Kalergis, Alexis M.

AU - Riedel, Claudia A.

PY - 2015/4/1

Y1 - 2015/4/1

N2 - 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.

AB - 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.

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U2 - 10.1210/en.2014-1371

DO - 10.1210/en.2014-1371

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