ArticleMolecular endocrinology (Baltimore, Md.)2011
Regulation of thyroid oxidative state by thioredoxin reductase has a crucial role in thyroid responses to iodide excess.
Article in Molecular endocrinology (Baltimore, Md.), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 69 citations in OpenAlex.
- Recent Advances in the Treatment of Thyroid Pathologies with Selenium-Containing Compounds, Nanoparticles and Nanocomplexes Based on Selenium and Selenoproteins.Biological trace element research · 2026Review
- Iodine and Its Impact on the Immune System of Humans and Domesticated Mammals: A Narrative Review.Nutrients · 2026Review
- Exploring the Impacts of Fluoride-Induced Thyroid Toxicity: A Comprehensive Review.Biological trace element research · 2026Review
- DNA Damage and Repair in Thyroid Physiology and Disease.Endocrine reviews · 2026Review
- Review
- 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
- Could Oxidative Stress Play a Role in the Development and Clinical Management of Differentiated Thyroid Cancer?Cancers · 2023Review
- Nrf2-Mediated Antioxidant Defense and Thyroid Hormone Signaling: A Focus on Cardioprotective Effects.Antioxidants (Basel, Switzerland) · 2023Review
- Protection of Vitamin C on Oxidative Damage Caused by Long-Term Excess Iodine Exposure in Wistar Rats.Nutrients · 2022Article
- Review
- Basolateral Sorting of the Sodium/Iodide Symporter Is Mediated by Adaptor Protein 1 Clathrin Adaptor Complexes.Thyroid : official journal of the American Thyroid Association · 2022Article
- The Impact of Kohlrabi Sprouts on Various Thyroid Parameters in Iodine Deficiency- and Sulfadimethoxine-Induced Hypothyroid Rats.Nutrients · 2022Article
- Thyroid Dysfunction and COVID-19: The Emerging Role of Selenium in This Intermingled Relationship.International journal of environmental research and public health · 2022Review
- Redox Homeostasis in Thyroid Cancer: Implications in NaInternational journal of molecular sciences · 2022Review
- Review
- Review
- The Transcriptomic Response of the Murine Thyroid Gland to Iodide Overload and the Role of the Nrf2 Antioxidant System.Antioxidants (Basel, Switzerland) · 2020Article
- HAntioxidants (Basel, Switzerland) · 2019Review
- NFE2-Related Transcription Factor 2 Coordinates Antioxidant Defense with Thyroglobulin Production and Iodination in the Thyroid Gland.Thyroid : official journal of the American Thyroid Association · 2018Article
Corrections and comments
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Authors and funding
4 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The phenomenon that supraphysiological doses of iodide (I(-)) temporarily inhibit thyroid hormone synthesis is known as thyroid iodide autoregulation. Recovery of thyroid function has been attributed to sodium-iodide symporter (NIS) inhibition, but the diversity of available data makes it difficult to reach definitive conclusions. Iodide excess induces reactive oxygen species production and cell toxicity. However, the roles of the oxidative state of the cell and antioxidant selenoproteins in I(-) autoregulation have never been explored. Here we analyze the effects of high I(-) doses in rat thyroids and in PCCl3 cells in the period comprising I(-) autoregulation (i.e. 0-72 h after I(-) administration), focusing on NIS expression, redox state, and the expression and activity of selenoproteins. Our results show that NIS mRNA inhibition by I(-) does not occur at the transcriptional level, because neither NIS promoter activity nor Pax8 expression or its binding to DNA was modulated. Because I(-) uptake was inhibited much earlier than NIS protein, and no effect was observed on its subcellular localization, we suggest that I(-) is inhibiting NIS in the plasma membrane. The increased reactive oxygen species production leads to an increase in thioredoxin reductase mRNA levels and enzyme activity, which reduces the oxidative stress. Inhibition of thioredoxin reductase at either gene expression or activity levels prevented NIS recovery, thus illustrating a new role played by this selenoprotein in the regulation of cell homeostasis and consequently in I(-) autoregulation.
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