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The Role of Oxidative Stress on the Pathogenesis of Graves' Disease

Graves' disease is a most common cause of hyperthyroidism. It is an autoimmune disease, and autoimmune process induces an inflammatory reaction, and reactive oxygen species (ROSs) are among its products. When balance between oxidants and antioxidants is disturbed, in favour of the oxidants it i...

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Autor principal: Žarković, Miloš
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi Publishing Corporation 2012
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3235898/
https://www.ncbi.nlm.nih.gov/pubmed/22175033
http://dx.doi.org/10.1155/2012/302537
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author Žarković, Miloš
author_facet Žarković, Miloš
author_sort Žarković, Miloš
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description Graves' disease is a most common cause of hyperthyroidism. It is an autoimmune disease, and autoimmune process induces an inflammatory reaction, and reactive oxygen species (ROSs) are among its products. When balance between oxidants and antioxidants is disturbed, in favour of the oxidants it is termed “oxidative stress” (OS). Increased OS characterizes Graves' disease. It seems that the level of OS is increased in subjects with Graves' ophthalmopathy compared to the other subjects with Graves' disease. Among the other factors, OS is involved in proliferation of orbital fibroblasts. Polymorphism of the 8-oxoG DNA N-glycosylase 1 (hOGG1) involved in repair of the oxidative damaged DNA increases in the risk for developing Grave's disease. Treatment with glucocorticoids reduces levels of OS markers. A recent large clinical trial evaluated effect of selenium on mild Graves' ophthalmopathy. Selenium treatment was associated with an improved quality of life and less eye involvement and slowed the progression of Graves' orbitopathy, compared to placebo.
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spelling pubmed-32358982011-12-15 The Role of Oxidative Stress on the Pathogenesis of Graves' Disease Žarković, Miloš J Thyroid Res Review Article Graves' disease is a most common cause of hyperthyroidism. It is an autoimmune disease, and autoimmune process induces an inflammatory reaction, and reactive oxygen species (ROSs) are among its products. When balance between oxidants and antioxidants is disturbed, in favour of the oxidants it is termed “oxidative stress” (OS). Increased OS characterizes Graves' disease. It seems that the level of OS is increased in subjects with Graves' ophthalmopathy compared to the other subjects with Graves' disease. Among the other factors, OS is involved in proliferation of orbital fibroblasts. Polymorphism of the 8-oxoG DNA N-glycosylase 1 (hOGG1) involved in repair of the oxidative damaged DNA increases in the risk for developing Grave's disease. Treatment with glucocorticoids reduces levels of OS markers. A recent large clinical trial evaluated effect of selenium on mild Graves' ophthalmopathy. Selenium treatment was associated with an improved quality of life and less eye involvement and slowed the progression of Graves' orbitopathy, compared to placebo. Hindawi Publishing Corporation 2012 2011-12-10 /pmc/articles/PMC3235898/ /pubmed/22175033 http://dx.doi.org/10.1155/2012/302537 Text en Copyright © 2012 Miloš Žarković. https://creativecommons.org/licenses/by/3.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Review Article
Žarković, Miloš
The Role of Oxidative Stress on the Pathogenesis of Graves' Disease
title The Role of Oxidative Stress on the Pathogenesis of Graves' Disease
title_full The Role of Oxidative Stress on the Pathogenesis of Graves' Disease
title_fullStr The Role of Oxidative Stress on the Pathogenesis of Graves' Disease
title_full_unstemmed The Role of Oxidative Stress on the Pathogenesis of Graves' Disease
title_short The Role of Oxidative Stress on the Pathogenesis of Graves' Disease
title_sort role of oxidative stress on the pathogenesis of graves' disease
topic Review Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3235898/
https://www.ncbi.nlm.nih.gov/pubmed/22175033
http://dx.doi.org/10.1155/2012/302537
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