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Written by: Medical Affairs Team

Length: 5 minute read

Posted:

  • Metabolic Health
  • Thyroid Health

Understanding Selenium and Iodine: Mechanisms and Functions

Understanding Selenium and Iodine: Mechanisms and Functions

by Yvonne Hart, MS, NBC-HWC

Key Takeaways

  • Iodine Function: Integral to thyroid hormone synthesis and metabolic regulation.*
  • Selenium Function: Supports redox balance, thyroid hormone activity, and normal cellular repair.*
  • Molecular Interplay: Selenium and iodine collaborate to maintain thyroid hormone homeostasis and support cellular integrity.*
  • Systemic Importance: These micronutrients influence processes far beyond the thyroid, extending their roles to immune function, energy metabolism, and cellular resilience.*

Selenium and iodine are vital trace minerals with surprisingly complex roles in human health. These molecular multitaskers are indispensable for maintaining thyroid function and supporting the body's antioxidant defenses. But how do they pull this off at the biochemical level? This article explores the intricate pathways of selenium and iodine, uncovering how their distinct functions converge to support health from the inside out.*

Iodine Function and Mechanism of Action

Iodine’s primary function is as a key component of thyroid hormones, thyroxine (T4), and triiodothyronine (T3). These hormones regulate metabolism, growth, and development by influencing the expression of numerous genes.[1] The journey of iodine through the body involves several fascinating molecular steps:

Absorption and Transport:

Dietary iodine is absorbed in the stomach and small intestine as iodide (I⁻). Once in circulation, iodide is transported to the thyroid gland via sodium-iodide symporters (NIS) on the basolateral membrane of thyrocytes, an essential process for thyroid hormone production.[2] 

Thyroid Hormone Synthesis:

In the thyroid gland, iodide is oxidized to iodine by the enzyme thyroid peroxidase (TPO). This activated iodine binds to tyrosine residues on thyroglobulin, forming monoiodotyrosine (MIT) and diiodotyrosine (DIT), which then couple to produce T4 and T3 for storage in the thyroid follicle until needed.*[3]

Release and Mechanism of Action: 

When required, thyroid hormones are released into the bloodstream. T4 is converted to the more active T3 by deiodinase enzymes, a process dependent on selenium (more on that later). T3 binds to nuclear receptors, influencing transcriptional activity and modulating metabolic processes.*[4]

Selenium Function and Mechanism of Action

Selenium is an essential, non-metallic mineral that supports redox balance, thyroid hormone metabolism, and cellular health through its incorporation into selenoproteins.*[5]

Selenium undergoes a complex metabolic pathway in the liver, where it is converted into selenocysteine, which is then incorporated into selenoproteins through a tightly regulated biological process essential for supporting cellular integrity and facilitating metabolic processes.*[6]

Redox Balance: 

Many selenoproteins, including glutathione peroxidases (GPx) and thioredoxin reductases, support cellular integrity.*5 These enzymes catalyze reactions that reduce hydrogen peroxide and lipid hydroperoxides to water and alcohols, maintaining redox homeostasis.* [7],[8]

Thyroid Hormone Metabolism:

Selenium-dependent deiodinases (DIO1, DIO2, and DIO3) regulate thyroid hormone activity.* These enzymes convert T4 to T3 or reverse T3 (rT3), fine-tuning thyroid hormone activity to match physiological demands.*[9]

The Interplay Between Selenium and Iodine

The functions of selenium and iodine are intricately linked, particularly within the thyroid gland. Adequate selenium levels are essential for the proper functioning of deiodinase enzymes, which activate thyroid hormones.6 Without sufficient selenium, T4 cannot efficiently convert to T3, which may impact normal thyroid hormone signaling.*[5]

Selenium-containing selenoproteins also support cellular integrity during thyroid hormone synthesis.

Selenoproteins

Selenoproteins are the molecular machinery that drive selenium’s functions. Selenoproteins play diverse roles in human physiology, driving key processes such as antioxidant defense, cellular repair, and immune system modulation. [5], [10]  Here’s a closer look:

  1. Glutathione Peroxidases (GPx): These enzymes catalyze the reduction of hydrogen peroxide and lipid hydroperoxides, supporting cellular redox balance.* [6]
  2. Thioredoxin Reductases (TXNRD): These enzymes help maintain antioxidants like thioredoxin in their active states, promoting cellular resilience and growth.*
  3. Selenoprotein P (SELENOP): Produced primarily in the liver, SELENOP transports selenium to various tissues, ensuring adequate selenium levels for cellular function.*
  4. Selenoprotein W (SELENOW): Found in muscle and heart tissues, SELENOW supports cellular redox balance and structural integrity.*
  5. Iodothyronine Deiodinases (DIO): These selenium-dependent enzymes regulate thyroid hormone activity, converting inactive T4 into the active T3.*
  6. Methionine Sulfoxide Reductase B1 (MSRB1): This enzyme repairs oxidized methionine residues in proteins, maintaining cellular integrity under oxidative stress.*
  7. Selenoprotein S (SELENOS): SELENOS supports cellular stress responses and immune system function.*

Selenium and Iodine in Systems Biology

Beyond their individual contributions, selenium and iodine are integral to broader physiological systems, including immune modulation, antioxidant defense, energy metabolism, and cellular repair. * [5],[11],[12]   Within the endocrine system, selenium and iodine coordinate to optimize thyroid hormone output and activity by supporting hormone synthesis, activation, antioxidant defense, regulation of hormone breakdown, and maintenance of hormonal homeostasis.*[12],[13]  Selenium’s antioxidant properties also extend their influence into the nervous and cardiovascular systems, supporting overall cellular resilience in these tissues.*[11]

Molecular studies emphasize the potential epigenetic roles of selenoproteins, such as modulating gene expression through redox-sensitive transcription factors. [14],[15]   Similarly, iodine’s impact on thyroid hormones indirectly influences mitochondrial biogenesis and energy homeostasis, underscoring the systemic nature of these minerals.*[16]

Conclusion

A deeper understanding of the molecular mechanisms of selenium and iodine highlights their indispensable roles in maintaining physiological balance. From optimizing thyroid hormone regulation to bolstering antioxidant defense and cellular repair, these trace minerals are integral to clinical strategies. Ensuring patients achieve adequate intake supports the complex biochemical pathways that contribute to their metabolic health and resilience.*

*These statements have not been evaluated by the Food and Drug Administration. This article is for informational purposes only and not intended to diagnose, treat, cure, or prevent any disease.

Yvonne Hart, MS, NBC-HWC is the founder of NuVida Wellness, focusing on empowering clients through evidence-based strategies in lifestyle modification, chronic disease management, and holistic wellness. She is a board-certified health and wellness coach and clinical nutrition applied scientist with a background in biology and over a decade of entrepreneurial experience. Yvonne completed her health and wellness coaching training at Duke Integrative Medicine and earned her Master of Science in Clinical Nutrition from Sonoran University of Health Sciences. 

[1] Galton VA, et al. Thyroid. 2021;31(3):528-41. doi:10.1089/thy.2020.0508

[2] Bizhanova A, Kopp P. Endocrinology. 2009;150(3):1084-90. 7

[3] Renko K, et al. Endocrinology. 2016;157(12):4516-25.

[4] Liu YY, Brent GA. Trends Endocrinol Metab. 2010;21(3):166-73. 4

[5] Zhang F, et al. Biomolecules. 2023;13(5):799. doi:10.3390/biom13050799

[6] Wang F, et al. Front Endocrinol (Lausanne). 2023;14:1133000. doi:10.3389/fendo.2023.1133000

[7] Arnér ESJ, Holmgren A. Semin Cancer Biol. 2006;16(6):420-26.

[8] Kang D, et al. Nat Commun. 2022;13:779. doi:10.1038/s41467-022-28385-7

[9] Köhrle J. Cell Mol Life Sci. 2000;57(13-14):1853-63. 7

[10] Avery JC, Hoffmann PR. Nutrients. 2018;10(9):1203. doi:10.3390/nu10091203

[11] Huang Z, et al. Antioxid Redox Signal. 2012;16(7):705-43.

[12] Köhrle J. Int J Mol Sci. 2023;24(4):3393. doi:10.3390/ijms24043393

[13] Schomburg L, Köhrle J. Mol Nutr Food Res. 2008;52(11):1235-46.

[14] Zhang Y, et al. Antioxidants (Basel). 2020;9(5):383. doi:10.3390/antiox9050383

[15] Narayan V, et al. J Nutr Biochem. 2015;26(2):138-45.

[16] Weitzel JM, et al. Exp Physiol. 2003;88(1):121-8.

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