scholarly journals Selenium in Hyperthyroidism

2020 ◽  
Vol 3 (2) ◽  
pp. 24
Author(s):  
Shiela Stefani ◽  
Lukman Halim ◽  
Diyah Eka Andayani ◽  
Fiastuti Witjaksono

Introduction: Thyroid gland has the highest selenium content compare with other endocrine organs. Enzyme that catalyzing thyroid hormone activation, iodothyronine deiodinases, were identified as selenocysteine-containing proteins. Selenium levels in soil and rice consumed in Indonesia were lower than in several other countries, which can increase the risk of selenium deficiency.Methods: This is an article review of the current literatures published up to November 2018 about the role of selenium in hyperthyroid.Result: Several studies have shown that selenium supplementation can be beneficial in patients with Graves disease and autoimmune thyroiditis. Selenium has an important immunomodulatory effect, but the effects of selenium supplementation in hyperthyroid has not been conclude. Data regarding selenium intake, prevalence of deficiency, and the relationship between selenium and thyroid disease in Indonesia are limited. Various studies of selenium supplementation in thyroid disease provide controversial results, so there are no guidelines that include selenium as standard therapy hyperthyroid. Selenium supplementation can enhance the restoration of biochemical euthyroidism in Graves disease and was associated with a significant decrease in the levels of thyroid peroxidase antibodies in autoimmune thyroiditis.Conclusions: Micronutrients that play a role in thyroid hormone synthesis and maintain thyroid function in addition to selenium are iodine, iron, zinc, and vitamin A. By correcting the deficit of selenium, and meeting other micronutrient requirements may provide health benefits in patient with hyperthyroid.

1927 ◽  
Vol 23 (1) ◽  
pp. 29-32
Author(s):  
M. N. Cheboksarov ◽  
Z. I. Malkin

The question of the relationship of the endocrine glands, and in particular the adrenal glands, to immunity has not yet been finally resolved: while some authors recognize only the indirect importance of the endocrine organs in the fight against infection, given the extremely extensive biological role of these organs in the life of the animal body, others are inclined to seek a more direct relationship, allowing their participation or in the production of antithelials, or in the neutralization of bacterial toxins.


2020 ◽  
Vol 223 (22) ◽  
pp. jeb237701
Author(s):  
Tushar S. Sirsat ◽  
Edward M. Dzialowski

ABSTRACTAt hatching in precocial birds, there are rapid physiological and metabolic phenotypic changes associated with attaining endothermy. During the transition to ex ovo life, thyroid hormone levels naturally increase, peaking at hatching, and then decline. To better understand the role of the natural increase in thyroid hormone at hatching in regulating the developmental trajectory of the Pekin duck's endothermic phenotype, we examined development of O2 consumption (V̇O2) and ventilation (frequency, tidal volume and minute ventilation) while inhibiting the developmental increase in thyroid hormones that occurs at hatching via administration of the thyroid-peroxidase inhibitor methimazole (MMI) or accelerating the developmental increase via triiodothyronine (T3) supplementation. Animals were dosed only on day 24 of a 28-day incubation period and studied on incubation day 25, during external pipping (EP) and 1 day post-hatching (dph). On day 25, there was an increase in V̇O2 in the hyperthyroid treatment compared with the other two treatments. During the EP stage, there was a significant effect of thyroid status on V̇O2, with hyperthyroid V̇O2 being highest and hypothyroid V̇O2 the lowest. By 1 dph, the supplemented T3 and control animals had similar V̇O2 responses to cooling with comparable thermal neutral zones followed by increased V̇O2. Hypothyroid 1 dph hatchlings had a lower resting V̇O2 that did not increase to the same extent as the supplemented T3 and control animals during cooling. During EP, inhibiting the rise in T3 resulted in embryos with lower ventilation frequency and tidal volume than control and supplemented T3 embryos. At 1 dph, ventilation frequency of all animals increased during cooling, but tidal volume only increased in supplemented T3 and control hatchlings. Our data support the role of the late incubation increase in T3 in regulating the systemic development of endothermic metabolic capacity and associated control of ventilation occurring at hatching of the Pekin duck.


2013 ◽  
Vol 154 (41) ◽  
pp. 1628-1635 ◽  
Author(s):  
Csaba Balázs ◽  
Károly Rácz

Oxygen derived free radicals, generated by a number of cellular reactions, include superoxide anion, hydrogen peroxide and hydroxyl radicals. They exert their cytotoxic effects mainly via peroxidation of the cell membrane resulting in the loss of membrane integrity. The essential trace element, selenium exerts complex effects on the endocrine systems, partly due to its antioxidant capacity. Well-characterized selenoproteins include iodothyronine deiodinases, glutathione peroxidases and thioredoxin reductases involved in thyroid hormone metabolism and protection from oxidative damage. The value of selenium supplementation in autoimmune thyroid disorders has been investigated and most studies confirmed the beneficial effect of selenium supplementation in Hashimoto’s and Graves’s diseases. Recently, selenium proved to be effective in mild inflammatory orbitopathy. There are a number of reports about the effect of selenium in diabetes mellitus, but the data are controversial as both insulin-like and diabetes-inducing effects of selenium have been described. Selenium was successfully used in both female and male infertility of autoimmune origin. Orv. Hetil., 154 (41), 1628–1635.


2005 ◽  
Vol 118 (2) ◽  
pp. 239-245 ◽  
Author(s):  
Alain VIRION ◽  
Danièale DEME ◽  
Jacques POMMIER ◽  
Jacques NUNEZ

1991 ◽  
Vol 69 (11) ◽  
pp. 1648-1652 ◽  
Author(s):  
John R. Arthur

In animals, decreases in selenium-containing glutathione peroxidase activity and the resultant impairment of peroxide metabolism can account for many, but not all of the biochemical and clinical changes caused by selenium deficiency. Recently, however, type I iodothyronine 5′-deiodinase has also been shown to be a selenium-containing enzyme. This explains the impairment of thyroid hormone metabolism caused by selenium deficiency in animals with a normal vitamin E status. Since iodothyronine 5′-deiodinases are essential for the production of the active thyroid hormone 3,5,3′-triiodothyronine, some of the consequences of selenium deficiency may result from thyroid changes rather than inability to metabolise peroxides. In particular, the impaired thyroid hormone metabolism may be responsible for decreased growth and resistance to cold stress in selenium-deficient animals. A further consequence of the role of selenium in thyroid hormone metabolism is the exacerbation of some of the thyroid changes in iodine deficiency by a concurrent selenium deficiency. Selenium status may therefore have a major influence on the outcome of iodine deficiency in both human and animal populations.Key words: selenium, thyroid hormones, iodothyronine deiodinases, iodine, nutritional disorders.


1972 ◽  
Vol 69 (2) ◽  
pp. 321-328
Author(s):  
K. Liewendahl ◽  
E. Niskanen ◽  
A. Gordin

ABSTRACT The effects of excess iodide on the histology and function of the thyroid were studied in rats. A slight increase in thyroid weight and minimal histological alterations were observed. The thyroid function of rats was studied by measuring the serum total and free thyroxine. Excess iodide did not significantly change the concentration of thyroid hormone in the serum and signs of hypothyroidism were not seen. Thus, rats were capable of adaptation to chronic administration of large amounts of iodide. A slight increase in the serum thyrotrophin after prolonged ingestion of excess iodide was measured with both bioassay and radioimmunoassay techniques. The possible role of thyrotrophin in the mechanism of escape from the transient inhibition of iodide on thyroid hormone synthesis is discussed.


2001 ◽  
pp. 561-568 ◽  
Author(s):  
M Andrikoula ◽  
A Tsatsoulis

Recent evidence has emphasized the importance of apoptosis in the maintenance of tissue homeostasis and the pathogenesis of malignant and immune diseases. Autoimmune thyroid diseases such as Hashimoto's thyroiditis and Graves' disease, as well as other autoimmune endocrine diseases, have been associated with dysregulation of apoptotic signaling pathways. In particular, dysfunction of the Fas apoptotic pathway or production of soluble factors including soluble Fas and soluble Fas ligand may be involved in the pathogenesis of these disorders. On the other hand, malignant thyroid cells may avoid Fas-mediated suicide possibly by expression of inhibitors of apoptosis and evade the immune system by inducing apoptosis on infiltrating lymphocytes. The delicate balance between cell proliferation and cell death through the Fas pathway may also play an important role in the control of thyroid cell mass and goitrogenesis. This review analyzes the current evidence on the role of Fas-mediated apoptosis in the pathogenesis of thyroid diseases including Hashimoto's thyroiditis, Graves' disease, thyroid cancer and goiter. However, the exact mechanisms involved in the regulation of apoptosis in thyroid disease remain unclear. Further investigation is needed.


2013 ◽  
Vol 5 (1) ◽  
pp. 5-11
Author(s):  
S Akhter ◽  
ZU Nahar ◽  
S Parvin ◽  
A Alam ◽  
S Sharmin ◽  
...  

Iron deficiency is the most important but preventable nutritional problem in Bangladesh. Thyroid peroxidase, an iron containing enzyme, is essential for initial two steps of thyroid hormone synthesis which is a component of tissue iron. Tissue iron diminishes early in the course of iron deficiency. So thyroid hormone level may be altered in iron deficient patients. This case-control study was carried out in the Department of Biochemistry, Bangabandhu Sheikh Mujib Medical University (BSMMU) from July 2006 to June 2007. This study was done to find out the changes of thyroid hormonal activity in iron deficiency.In this study 72 subjects were selected from the out-patient department of the hospital. Patients with low serum ferritin level <12 mgm/L were selected as cases (n=36) and healthy persons with normal serum ferritin level were taken as controls. Serum ferritin, thyroid stimulating hormone (TSH), free thyroxine (FT4) and free triiodothyronine (FT3) were measured in all study subjects. Values were expressed as mean ± SD. Unpaired 't' test and Pearson's correlation test were performed to see the level of significance and p value <0.05 was taken as significant. Serum ferritin level in cases and controls were 6.78±4.05 mgm/L and 79.04±28.08 mgm/L respectively which showed significant difference (P<0.0001).Serum TSH concentration in cases and controls were 3.32±1.54 mIU/L and 1.89±0.86 mIU/L respectively. Serum FT4 concentration in cases and controls were 11.66±1.77 pmol/L and 13/10±1.36 pmol/L respectively and that of FT3 were 3.00±0.68 and 3.31±0.61 pmol/L respectively. All showed significant difference between groups.Serum ferritin and Serum TSH showed significant negative correlation in controls whereas in cases they showed negative correlation which was not statistically significant.Both serum FT4 and FT3 revealed positive correlation with serum ferritin but that too was not significant statistically.Though the study failed to show any significant positive correlation between serum ferritin and thyroid hormones, lower level of thyroid status in iron deficient patients suggest that it could be a reflection of disturbed activities of iron dependent enzymes such as thyroid peroxidase that impairs thyroid hormone synthesis. However, a large scale study is recommeded to establish the fact.This study showed that there was significant difference in thyroid hormonal status between iron deficient patients and normal healthy persons. Therefore it can be concluded that iron deficiency may impair normal thyroid hormone status. DOI: http://dx.doi.org/10.3329/bjmb.v5i1.13424 Bangladesh J Med Biochem 2012; 5(1): 5-11


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