ArticleEndocrinology2015
Excess iodide induces an acute inhibition of the sodium/iodide symporter in thyroid male rat cells by increasing reactive oxygen species.
Article in Endocrinology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
16 citing papers in PubMed, 1 synthesis or guideline pooled it, 43 citations in OpenAlex.
- The potential interaction between medical treatment and radioiodine treatment success: A systematic review.Frontiers in endocrinology · 2022Pooled it
- Mechanistic insights into PFAS-induced toxicity: from lipid membrane perturbation to ion channel and transporter dysregulation.Archives of toxicology · 2026Review
- Implications of Endocrine-Disrupting Chemicals for Human Health and Effective Methods for Prevention and Reduction.Toxics · 2026Review
- Micro- and Nanoplastics as Disruptors of the Endocrine System-A Review of the Threats and Consequences Associated with Plastic Exposure.International journal of molecular sciences · 2025Review
- Chloride channel-3 regulates sodium-iodide symporter expression and localization in the thyroids of mice on a high-iodide diet.Frontiers in nutrition · 2025Article
- Review of the PRIODAC project on thyroid protection from radioactive iodine by repeated iodine intake in individuals aged 12.European thyroid journal · 2024Review
- Exogenous Melatonin Protects against Oxidative Damage to Membrane Lipids Caused by Some Sodium/Iodide Symporter Inhibitors in the Thyroid.Antioxidants (Basel, Switzerland) · 2023Article
- Review
- Redox Homeostasis in Thyroid Cancer: Implications in NaInternational journal of molecular sciences · 2022Review
- Targeting non-canonical pathways as a strategy to modulate the sodium iodide symporter.Cell chemical biology · 2022Article
- Effect of Dietary Seaweed Supplementation in Cows on Milk Macrominerals, Trace Elements and Heavy Metal Concentrations.Foods (Basel, Switzerland) · 2021Article
- Review
- [Iodine-rich thermal water in cure and rehabilitation from the perspective of the thyroid gland].Wiener medizinische Wochenschrift (1946) · 2020Article
- HAntioxidants (Basel, Switzerland) · 2019Review
- Overexpression of Interleukin-4 in the Thyroid of Transgenic Mice Upregulates the Expression of Duox1 and the Anion Transporter Pendrin.Thyroid : official journal of the American Thyroid Association · 2016Article
- Iodide excess regulates its own efflux: a possible involvement of pendrin.American journal of physiology. Cell physiology · 2016Article
Corrections and comments
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Authors and funding
13 authors at 4 institutions in 3 countries.
Funding
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.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.