A Comprehensive Review of Selenium as a Key Regulator in Thyroid Health

Abstract

Selenium (Se) is an essential trace element crucial for thyroid function, participating in the production and metabolism of thyroid hormones and the immune system. It engages in synthesizing selenoproteins, which are essential for antioxidant defense and regulating thyroid hormone levels. It is crucial to convert thyroxine (T4) into the active thyroid hormone triiodothyronine (T3) via deiodinase activity and safeguard thyroid cells from oxidative damage. Therefore, thyroid dysfunction, including abnormalities in thyroid hormone synthesis and the emergence of autoimmune thyroid conditions such as Graves' disease and Hashimoto's thyroiditis, has been linked to Se deficiency. When evaluating the benefits of Se supplementation, it is crucial to recognize that excessive mineral intake may be detrimental and result in adverse consequences, including gastrointestinal disturbances and neurological problems. The effectiveness of Se-based therapies is influenced by individual characteristics, including hereditary anomalies in thyroid function and Se metabolism. Further research should be performed on personalized Se supplementation approaches using genetics and nanotechnology to optimize the bioavailability and efficacy of the supplements. This study aims to thoroughly examine Se's role in thyroid health and how its therapeutic use in thyroid-related diseases may be optimized via appropriate dosing.

Keywords: Oxidative stress; Selenium; Selenoproteins; Thyroid gland and hormones; Trace mineral.

Fig. 1

Effect of low Se and TXNRD1 deficiency on thyroid gland OS pathways. Particularly its impact on the expression of thioredoxin reductase 1 (TXNRD1), a fundamental selenoenzyme involved in redox control; this figure shows the molecular and cellular repercussions of Se deprivation. Low Se levels reduce TXNRD1 activity in the thyroid, upsetting antioxidant protection and raising OS susceptibility. Among the many sources of ROS shown are NADPH oxidase activation, microbial absorption, radiation exposure, endoplasmic reticulum (ER) stress, mitochondrial oxidative phosphorylation, and peroxisomal metabolism. In the lack of enough Se-mediated enzymatic detoxification, the buildup of ROS, including hydrogen peroxide (H₂O₂) and superoxide (O₂,⁻ causes cellular damage and thyroid malfunction. This route emphasizes the role TXNRD1 and selenium play in preserving redox balance and shielding thyroid tissue from oxidative damage

Fig. 2

The relative functions of the thyroid and SelPs synthesis via SeMet’s metabolic routes. SelPs production and the metabolic fate of dietary Se molecules, especially SeMet, are shown in this graphic. To get to selenocysteine, the trans-sulfuration route converts SeMet via stages that include selenocystathionine. The synthesis of SelPs is subsequently facilitated by selnocysteine via Sec-tRNA. Melylselenol (CH₃SeH) is another possible intermediate in the Se homeostasis and excretion pathways; it may be further transformed to dimethyl selenide ((CH₃)₂Se) or trimethylselenonium ((CH₃)₃Se⁺). The glutathione system is shown to reduce inorganic Se forms like selenate (SeO₄²⁻) and selenite (SeO₃²⁻) to hydrogen selenide (H₂Se), a commonly used precursor for SelPs production. In addition, the graphic shows how selenium helps the thyroid gland’s SelPs with redox control and thyroid hormone metabolism, such as changing thyroxine (T₄) into triiodothyronine (T₃), the active form of thyroid hormone. This route shows the significance of SeMet as an endocrine regulator and antioxidant

Fig. 3

Challenges in Se-based thyroid therapies. In terms of Se in thyroid treatments, this conceptual picture identifies four main drawbacks: (1) A narrow therapeutic window exists for selenium supplementation because toxic consequences or adverse effects on thyroid hormone control and redox balance may result from either a deficit or an excess of the mineral; (2) Individual variations in SeLPs gene expression, polymorphisms, and enzymatic activity impact Se usage and treatment response, making routine dosage regimens more complicated due to genetic variability in Se metabolism; (3) The effectiveness of Se supplements is very variable due to factors such as the chemical type of the supplement (organic vs. inorganic), the amount of Se in the food, and the amount of selenium in the environment; (4) By improving stability, cellular absorption, and site-specific antioxidant effects, new methods using SeNPs and tailored delivery systems seek to circumvent conventional obstacles in precision medicine. The future of tailored Se supplementation for thyroid and OS-related diseases lies in these approaches