Selenium nutritional status and thyroid dysfunction

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Abstract

Selenium(Se) is an essential micronutrient for several immune and regulatory functions in the body. In thyroid tissue, Se contributes to the antioxidant system and is a crucial component of deiodinases, which are selenoproteins that participate in thyroid hormone metabolism. Additionally, this micronutrient exerts a significant impact on thyroid pathophysiology, as low levels of Se lead to reduced activity of glutathione peroxidase, a selenoprotein involved in antioxidative processes, thereby resulting in increased oxidative stress and damage to thyroid tissue. Selenium deficiency (SeD) can cause growth retardation and reproductive failure; in women and children, it may result in Keshan’s disease and Kashin-Beck’s disease. Research has shown an inverse correlation between Se serum levels and autoimmune thyroiditis in areas with mild SeD. In Graves’ disease, Se supplementation has been linked to faster achievement of euthyroidism as well as improvements in quality of life, lessened orbital involvement, and slower ocular progression of the disease. Furthermore, several studies suggest an association between serum SeD and the development of thyroid cancer. Maintaining physiological Se concentrations appears to be related to the prevention of thyroid disease, although current data are insufficient to conclusively support or refute the efficacy of supplementation. Through this narrative review, we aim to present the latest information on the role of selenium in thyroid pathophysiology. To identify relevant literature, specific search strategies were employed in the electronic databases PubMed, Lilacs, and SciELO.

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Molecular mechanisms of the Keap1–Nrf2 pathway in stress response and cancer evolution.

Keiko Taguchi, Hozumi Motohashi, Masayuki Yamamoto (2011)

The Keap1–Nrf2 regulatory pathway plays a central role in the protection of cells against oxidative and xenobiotic damage. Under unstressed conditions, Nrf2 is constantly ubiquitinated by the Cul3–Keap1 ubiquitin E3 ligase complex and rapidly degraded in proteasomes. Upon exposure to electrophilic and oxidative stresses, reactive cysteine residues of Keap1 become modified, leading to a decline in the E3 ligase activity, stabilization of Nrf2 and robust induction of a battery of cytoprotective genes. Biochemical and structural analyses have revealed that the intact Keap1 homodimer forms a cherry-bob structure in which one molecule of Nrf2 associates with two molecules of Keap1 by using two binding sites within the Neh2 domain of Nrf2. This two-site binding appears critical for Nrf2 ubiquitination. In many human cancers, missense mutations in KEAP1 and NRF2 genes have been identified. These mutations disrupt the Keap1–Nrf2 complex activity involved in ubiquitination and degradation of Nrf2 and result in constitutive activation of Nrf2. Elevated expression of Nrf2 target genes confers advantages in terms of stress resistance and cell proliferation in normal and cancer cells. Discovery and development of selective Nrf2 inhibitors should make a critical contribution to improved cancer therapy.

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THE 2021 EUROPEAN GROUP ON GRAVES’ ORBITOPATHY (EUGOGO) CLINICAL PRACTICE GUIDELINES FOR THE MEDICAL MANAGEMENT OF GRAVES’ ORBITOPATHY

Luigi Bartalena, George J. Kahaly, Lelio Baldeschi … (2021)

Graves’ orbitopathy (GO) is the main extrathyroidal manifestation of Graves’ disease (GD). Choice of treatment should be based on assessment of clinical activity and severity of GO. Early referral to specialized centers is fundamental for most patients with GO. Risk factors include smoking, thyroid dysfunction, high serum level of thyrotropin receptor antibodies, radioactive iodine (RAI) treatment, and hypercholesterolemia. In mild and active GO, control of risk factors, local treatments and selenium (selenium-deficient areas) are usually sufficient; if RAI treatment is selected to manage GD, low-dose oral prednisone prophylaxis is needed, especially if risk factors coexist. For both active moderate-to-severe and sight threatening GO, antithyroid drugs are preferred when managing Graves’ hyperthyroidism. In moderate-to-severe and active GO, intravenous (iv) glucocorticoids are more effective and better tolerated than oral glucocorticoids. Based on current evidence and efficacy/safety profile, costs and reimbursement, drug availability, long-term effectiveness and patient choice after extensive counselling, a combination of iv methylprednisolone and mycophenolate sodium is recommended as first-line treatment. A cumulative dose of 4.5 grams (g) of iv methylprednisolone in 12 weekly infusions is the optimal regimen. Alternatively, higher cumulative doses not exceeding 8 g can be used as monotherapy in most severe cases and constant/inconstant diplopia. Second-line treatments for moderate-to-severe and active GO include: a) a second course of iv methylprednisolone (7.5 g) subsequent to careful ophthalmic and biochemical evaluation, b) oral prednisone/prednisolone combined with either cyclosporine or azathioprine; c) orbital radiotherapy combined with oral or iv glucocorticoids, d) teprotumumab; e) rituximab and f) tocilizumab. Sight threatening GO is treated with several high single doses of iv methylprednisolone per week and, if unresponsive, with urgent orbital decompression. Rehabilitative surgery (orbital decompression, squint and eyelid surgery) is indicated for inactive residual GO manifestations.

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Biochemistry, cellular and molecular biology, and physiological roles of the iodothyronine selenodeiodinases.

Antonio Bianco, Domenico Salvatore, Balázs Gereben … (2002)

The goal of this review is to place the exciting advances that have occurred in our understanding of the molecular biology of the types 1, 2, and 3 (D1, D2, and D3, respectively) iodothyronine deiodinases into a biochemical and physiological context. We review new data regarding the mechanism of selenoprotein synthesis, the molecular and cellular biological properties of the individual deiodinases, including gene structure, mRNA and protein characteristics, tissue distribution, subcellular localization and topology, enzymatic properties, structure-activity relationships, and regulation of synthesis, inactivation, and degradation. These provide the background for a discussion of their role in thyroid physiology in humans and other vertebrates, including evidence that D2 plays a significant role in human plasma T(3) production. We discuss the pathological role of D3 overexpression causing "consumptive hypothyroidism" as well as our current understanding of the pathophysiology of iodothyronine deiodination during illness and amiodarone therapy. Finally, we review the new insights from analysis of mice with targeted disruption of the Dio2 gene and overexpression of D2 in the myocardium.

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Author and article information

Contributors

Luciana Sant’Ana Leone de Souza:

ORCID: http://orcid.org/0000-0003-2595-0603

Role: conceived the original ideaRole: wrote the paperRole: contributed to the final manuscript

Renata de Oliveira Campos:

ORCID: http://orcid.org/0000-0002-2888-4798

Role: conceived the original ideaRole: wrote the paperRole: contributed to the final manuscript

Jair de Souza Braga Filho:

ORCID: http://orcid.org/0000-0003-3846-7725