Sodium selenite supplementation does not fully restore oxidative stress-induced deiodinase dysfunction : implications for the nonthyroidal illness syndrome
Autor(a) principal: | |
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Data de Publicação: | 2015 |
Outros Autores: | , , |
Tipo de documento: | Artigo |
Idioma: | eng |
Título da fonte: | Repositório Institucional da UFRGS |
Texto Completo: | http://hdl.handle.net/10183/182273 |
Resumo: | Nonthyroidal illness syndrome (NTIS) is marked by low T3 and high reverse T3 levels. The physio- pathology is poorly understood but involves oxidative stress-induced disruption of the iodothyronine deiodinases, which activate or inactivate thyroid hormones. Selenium, an essential trace element, exerts antioxidant function mainly through the thioredoxin reductase (TRx) and glutathione peroxidase (GPx) redox-regulating systems. We evaluated the effect of sodium selenite on IL6-induced disruption on deiodinase function. Cell lines expressing endogenous deiodinases type 1(D1), 2(D2) or 3(D3) (HepG2, MSTO, and MCF-7 cells, respectively) were used in an intact cell model that mimics the deiodination process under physiological conditions of substrate and cofactor, in the presence or not of IL6, with or without selenite. Deiodinase activity was quantified by the amount of iodine-125 in the medium (D1 and D2) or by ion-exchange chromatography (D3). Oxidative stress was evaluated by measuring reactive species (RS), carbonyl content as well as enzymatic and non-enzymatic antioxidant defenses. Results: IL6 induced ROS and carbonyl content in all 3 cell lines (all P o 0.001). Increased ROS was paralleled by D1 and D2-decreased T3-production (P o 0.01) and increased D3-catalyzed T3-inactivation (P o 0.001). Se- lenite decreases the IL6-induced ROS and carbonyl content, while enhances Gpx and Trx activities. Nevertheless, it failed on restoring D1 or D2 function and only attenuates D3 activation (P o 0.05). In conclusion, although sodium selenite reduces IL6-induced redox imbalance it does not fully repair deiodinase function. These results shed light on NTIS physiopathology and might explain why low T3 levels are unaffected by selenium supplementation in sick patients. |
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Wajner, Simone MagagninRohenkohl, Helena CecinSerrano, Túlio Macário GracchoMaia, Ana Luiza Silva2018-09-20T02:29:22Z20152213-2317http://hdl.handle.net/10183/182273001076660Nonthyroidal illness syndrome (NTIS) is marked by low T3 and high reverse T3 levels. The physio- pathology is poorly understood but involves oxidative stress-induced disruption of the iodothyronine deiodinases, which activate or inactivate thyroid hormones. Selenium, an essential trace element, exerts antioxidant function mainly through the thioredoxin reductase (TRx) and glutathione peroxidase (GPx) redox-regulating systems. We evaluated the effect of sodium selenite on IL6-induced disruption on deiodinase function. Cell lines expressing endogenous deiodinases type 1(D1), 2(D2) or 3(D3) (HepG2, MSTO, and MCF-7 cells, respectively) were used in an intact cell model that mimics the deiodination process under physiological conditions of substrate and cofactor, in the presence or not of IL6, with or without selenite. Deiodinase activity was quantified by the amount of iodine-125 in the medium (D1 and D2) or by ion-exchange chromatography (D3). Oxidative stress was evaluated by measuring reactive species (RS), carbonyl content as well as enzymatic and non-enzymatic antioxidant defenses. Results: IL6 induced ROS and carbonyl content in all 3 cell lines (all P o 0.001). Increased ROS was paralleled by D1 and D2-decreased T3-production (P o 0.01) and increased D3-catalyzed T3-inactivation (P o 0.001). Se- lenite decreases the IL6-induced ROS and carbonyl content, while enhances Gpx and Trx activities. Nevertheless, it failed on restoring D1 or D2 function and only attenuates D3 activation (P o 0.05). In conclusion, although sodium selenite reduces IL6-induced redox imbalance it does not fully repair deiodinase function. These results shed light on NTIS physiopathology and might explain why low T3 levels are unaffected by selenium supplementation in sick patients.application/pdfengRedox biology. Amsterdam. Vol. 6 (Dec. 2015), p. 436-445Síndromes do eutireóideo doenteEspécies reativas de oxigênioEstresse oxidativoCarbonilação proteicaSelenito de sódioDeiodinasesSodium seleniteThyroidhormoneNonthyroidalillnesssyndromeSodium selenite supplementation does not fully restore oxidative stress-induced deiodinase dysfunction : implications for the nonthyroidal illness syndromeEstrangeiroinfo:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/openAccessreponame:Repositório Institucional da UFRGSinstname:Universidade Federal do Rio Grande do Sul (UFRGS)instacron:UFRGSORIGINAL001076660.pdfTexto completo (inglês)application/pdf2794216http://www.lume.ufrgs.br/bitstream/10183/182273/1/001076660.pdf9f96562be1ac46bfca329510934e7290MD51TEXT001076660.pdf.txt001076660.pdf.txtExtracted Texttext/plain46588http://www.lume.ufrgs.br/bitstream/10183/182273/2/001076660.pdf.txtebd2a55f5a5d720e8ed6a73865c25774MD52THUMBNAIL001076660.pdf.jpg001076660.pdf.jpgGenerated Thumbnailimage/jpeg1893http://www.lume.ufrgs.br/bitstream/10183/182273/3/001076660.pdf.jpga1b8d07dd0700cad82c1fb65819b23f6MD5310183/1822732024-03-13 05:04:15.334696oai:www.lume.ufrgs.br:10183/182273Repositório de PublicaçõesPUBhttps://lume.ufrgs.br/oai/requestopendoar:2024-03-13T08:04:15Repositório Institucional da UFRGS - Universidade Federal do Rio Grande do Sul (UFRGS)false |
dc.title.pt_BR.fl_str_mv |
Sodium selenite supplementation does not fully restore oxidative stress-induced deiodinase dysfunction : implications for the nonthyroidal illness syndrome |
title |
Sodium selenite supplementation does not fully restore oxidative stress-induced deiodinase dysfunction : implications for the nonthyroidal illness syndrome |
spellingShingle |
Sodium selenite supplementation does not fully restore oxidative stress-induced deiodinase dysfunction : implications for the nonthyroidal illness syndrome Wajner, Simone Magagnin Síndromes do eutireóideo doente Espécies reativas de oxigênio Estresse oxidativo Carbonilação proteica Selenito de sódio Deiodinases Sodium selenite Thyroidhormone Nonthyroidalillnesssyndrome |
title_short |
Sodium selenite supplementation does not fully restore oxidative stress-induced deiodinase dysfunction : implications for the nonthyroidal illness syndrome |
title_full |
Sodium selenite supplementation does not fully restore oxidative stress-induced deiodinase dysfunction : implications for the nonthyroidal illness syndrome |
title_fullStr |
Sodium selenite supplementation does not fully restore oxidative stress-induced deiodinase dysfunction : implications for the nonthyroidal illness syndrome |
title_full_unstemmed |
Sodium selenite supplementation does not fully restore oxidative stress-induced deiodinase dysfunction : implications for the nonthyroidal illness syndrome |
title_sort |
Sodium selenite supplementation does not fully restore oxidative stress-induced deiodinase dysfunction : implications for the nonthyroidal illness syndrome |
author |
Wajner, Simone Magagnin |
author_facet |
Wajner, Simone Magagnin Rohenkohl, Helena Cecin Serrano, Túlio Macário Graccho Maia, Ana Luiza Silva |
author_role |
author |
author2 |
Rohenkohl, Helena Cecin Serrano, Túlio Macário Graccho Maia, Ana Luiza Silva |
author2_role |
author author author |
dc.contributor.author.fl_str_mv |
Wajner, Simone Magagnin Rohenkohl, Helena Cecin Serrano, Túlio Macário Graccho Maia, Ana Luiza Silva |
dc.subject.por.fl_str_mv |
Síndromes do eutireóideo doente Espécies reativas de oxigênio Estresse oxidativo Carbonilação proteica Selenito de sódio |
topic |
Síndromes do eutireóideo doente Espécies reativas de oxigênio Estresse oxidativo Carbonilação proteica Selenito de sódio Deiodinases Sodium selenite Thyroidhormone Nonthyroidalillnesssyndrome |
dc.subject.eng.fl_str_mv |
Deiodinases Sodium selenite Thyroidhormone Nonthyroidalillnesssyndrome |
description |
Nonthyroidal illness syndrome (NTIS) is marked by low T3 and high reverse T3 levels. The physio- pathology is poorly understood but involves oxidative stress-induced disruption of the iodothyronine deiodinases, which activate or inactivate thyroid hormones. Selenium, an essential trace element, exerts antioxidant function mainly through the thioredoxin reductase (TRx) and glutathione peroxidase (GPx) redox-regulating systems. We evaluated the effect of sodium selenite on IL6-induced disruption on deiodinase function. Cell lines expressing endogenous deiodinases type 1(D1), 2(D2) or 3(D3) (HepG2, MSTO, and MCF-7 cells, respectively) were used in an intact cell model that mimics the deiodination process under physiological conditions of substrate and cofactor, in the presence or not of IL6, with or without selenite. Deiodinase activity was quantified by the amount of iodine-125 in the medium (D1 and D2) or by ion-exchange chromatography (D3). Oxidative stress was evaluated by measuring reactive species (RS), carbonyl content as well as enzymatic and non-enzymatic antioxidant defenses. Results: IL6 induced ROS and carbonyl content in all 3 cell lines (all P o 0.001). Increased ROS was paralleled by D1 and D2-decreased T3-production (P o 0.01) and increased D3-catalyzed T3-inactivation (P o 0.001). Se- lenite decreases the IL6-induced ROS and carbonyl content, while enhances Gpx and Trx activities. Nevertheless, it failed on restoring D1 or D2 function and only attenuates D3 activation (P o 0.05). In conclusion, although sodium selenite reduces IL6-induced redox imbalance it does not fully repair deiodinase function. These results shed light on NTIS physiopathology and might explain why low T3 levels are unaffected by selenium supplementation in sick patients. |
publishDate |
2015 |
dc.date.issued.fl_str_mv |
2015 |
dc.date.accessioned.fl_str_mv |
2018-09-20T02:29:22Z |
dc.type.driver.fl_str_mv |
Estrangeiro info:eu-repo/semantics/article |
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info:eu-repo/semantics/publishedVersion |
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article |
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publishedVersion |
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http://hdl.handle.net/10183/182273 |
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2213-2317 |
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001076660 |
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http://hdl.handle.net/10183/182273 |
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eng |
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Redox biology. Amsterdam. Vol. 6 (Dec. 2015), p. 436-445 |
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openAccess |
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