Biochemical changes during goiter induction by methylmercaptoimidazol and inhibition by δ-iodolactone in rat

Autores
Thomasz, Lisa; Oglio, Andrea Romina; Randi, Andrea Silvana; Fernandez, Marina Olga; Dagrosa, Maria Alejandra; Cabrini, Romulo L.; Juvenal, Guillermo Juan; Pisarev, Mario Alberto
Año de publicación
2010
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
Background: We have demonstrated that the administration of δ-iodolactone (i.e., 5-iodo-delta lactone) of arachidonic acid (IL-δ), a mediator in thyroid autoregulation, prevents goiter induction by methylmercaptoimidazol (MMI) in rats. Other studies have shown that transforming growth factor beta-1 (TGF-β1) mimics some of the actions of excess iodide, but its participation in autoregulation is disputed. The present studies were performed to test the hypotheses that IL-δ decreases thyroid growth by inhibition of cell proliferation and/or by stimulation of apoptosis due to oxidative stress, that TGF-β is stimulated by an excess of iodide and by IL-δ, and that c-Myc and c-Fos expression are upregulated during goiter induction and downregulated during goiter inhibition. Methods: Rats were treated with MMI alone or together with iodide or IL-δ. Thyroid weight, cell number, cell proliferation, apoptosis, and oxidative stress were determined. Proliferating cell nuclear antigen (PCNA), TGF-β1, TGF-β3, c-Myc, and c-Fos were measured by Western blot. Results: MMI caused a progressive increase in thyroid weight accompanied by an increase in cell number, asymmetry of the ploidy histograms, and PCNA, c-Fos, and c-Myc expression. In addition, an early increase of apoptosis was observed. Peroxides as well as glutathione peroxidase and catalase activities were also increased in goitrous animals. The inhibitory action of IL-δ on goiter formation was accompanied by the inhibition of cell proliferation evidenced by a significant decrease in cell number, PCNA expression, and asymmetry of the ploidy histograms. A transient stimulation of apoptosis after 7 days of treatment was also observed. MMI administration stimulated TGF-β1 but not TGF-β3 synthesis. IL-δ alone caused a slight increase of TGF-β3 but not TGF-β1, whereas potassium iodide (KI) stimulated both isoforms and MMI reversed KI effect on TGF-β1 expression but not on TGF-β3. Conclusions: The goiter inhibitory action of IL-δ is due to the inhibition of cell proliferation and the transient stimulation of apoptosis. This latter action does not involve oxidative stress. TGF-β1 does not play a role in the autoregulatory pathway mediated by IL-δ. Iodide stimulates TGF-β3 without the need of being organified. These results suggest that there may be more than one pathway involved in the autoregulatory mechanism.
Fil: Thomasz, Lisa. Comision Nacional de Energía Atómica. Gerencia de Área de Aplicaciones de la Tecnología Nuclear. División Bioquímica Nuclear; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Oglio, Andrea Romina. Comision Nacional de Energía Atómica. Gerencia de Área de Aplicaciones de la Tecnología Nuclear. División Bioquímica Nuclear; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Randi, Andrea Silvana. Universidad de Buenos Aires. Facultad de Medicina. Departamento de Bioquímica Humana; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Fernandez, Marina Olga. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Dagrosa, Maria Alejandra. Comision Nacional de Energía Atómica. Gerencia de Área de Aplicaciones de la Tecnología Nuclear. División Bioquímica Nuclear; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Cabrini, Romulo L.. Comision Nacional de Energía Atómica. Gerencia de Área de Aplicaciones de la Tecnología Nuclear. División Bioquímica Nuclear; Argentina
Fil: Juvenal, Guillermo Juan. Comision Nacional de Energía Atómica. Gerencia de Área de Aplicaciones de la Tecnología Nuclear. División Bioquímica Nuclear; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Pisarev, Mario Alberto. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; Argentina. Comision Nacional de Energía Atómica. Gerencia de Área de Aplicaciones de la Tecnología Nuclear. División Bioquímica Nuclear; Argentina
Materia
Thyroid
Iodolipid
Autorregulation
Nivel de accesibilidad
acceso abierto
Condiciones de uso
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
Repositorio
CONICET Digital (CONICET)
Institución
Consejo Nacional de Investigaciones Científicas y Técnicas
OAI Identificador
oai:ri.conicet.gov.ar:11336/16264
Acceder
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network_acronym_str CONICETDig
repository_id_str 3498
network_name_str CONICET Digital (CONICET)
spelling Biochemical changes during goiter induction by methylmercaptoimidazol and inhibition by δ-iodolactone in ratThomasz, LisaOglio, Andrea RominaRandi, Andrea SilvanaFernandez, Marina OlgaDagrosa, Maria AlejandraCabrini, Romulo L.Juvenal, Guillermo JuanPisarev, Mario AlbertoThyroidIodolipidAutorregulationhttps://purl.org/becyt/ford/3.1https://purl.org/becyt/ford/3Background: We have demonstrated that the administration of δ-iodolactone (i.e., 5-iodo-delta lactone) of arachidonic acid (IL-δ), a mediator in thyroid autoregulation, prevents goiter induction by methylmercaptoimidazol (MMI) in rats. Other studies have shown that transforming growth factor beta-1 (TGF-β1) mimics some of the actions of excess iodide, but its participation in autoregulation is disputed. The present studies were performed to test the hypotheses that IL-δ decreases thyroid growth by inhibition of cell proliferation and/or by stimulation of apoptosis due to oxidative stress, that TGF-β is stimulated by an excess of iodide and by IL-δ, and that c-Myc and c-Fos expression are upregulated during goiter induction and downregulated during goiter inhibition. Methods: Rats were treated with MMI alone or together with iodide or IL-δ. Thyroid weight, cell number, cell proliferation, apoptosis, and oxidative stress were determined. Proliferating cell nuclear antigen (PCNA), TGF-β1, TGF-β3, c-Myc, and c-Fos were measured by Western blot. Results: MMI caused a progressive increase in thyroid weight accompanied by an increase in cell number, asymmetry of the ploidy histograms, and PCNA, c-Fos, and c-Myc expression. In addition, an early increase of apoptosis was observed. Peroxides as well as glutathione peroxidase and catalase activities were also increased in goitrous animals. The inhibitory action of IL-δ on goiter formation was accompanied by the inhibition of cell proliferation evidenced by a significant decrease in cell number, PCNA expression, and asymmetry of the ploidy histograms. A transient stimulation of apoptosis after 7 days of treatment was also observed. MMI administration stimulated TGF-β1 but not TGF-β3 synthesis. IL-δ alone caused a slight increase of TGF-β3 but not TGF-β1, whereas potassium iodide (KI) stimulated both isoforms and MMI reversed KI effect on TGF-β1 expression but not on TGF-β3. Conclusions: The goiter inhibitory action of IL-δ is due to the inhibition of cell proliferation and the transient stimulation of apoptosis. This latter action does not involve oxidative stress. TGF-β1 does not play a role in the autoregulatory pathway mediated by IL-δ. Iodide stimulates TGF-β3 without the need of being organified. These results suggest that there may be more than one pathway involved in the autoregulatory mechanism.Fil: Thomasz, Lisa. Comision Nacional de Energía Atómica. Gerencia de Área de Aplicaciones de la Tecnología Nuclear. División Bioquímica Nuclear; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Oglio, Andrea Romina. Comision Nacional de Energía Atómica. Gerencia de Área de Aplicaciones de la Tecnología Nuclear. División Bioquímica Nuclear; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Randi, Andrea Silvana. Universidad de Buenos Aires. Facultad de Medicina. Departamento de Bioquímica Humana; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Fernandez, Marina Olga. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Dagrosa, Maria Alejandra. Comision Nacional de Energía Atómica. Gerencia de Área de Aplicaciones de la Tecnología Nuclear. División Bioquímica Nuclear; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Cabrini, Romulo L.. Comision Nacional de Energía Atómica. Gerencia de Área de Aplicaciones de la Tecnología Nuclear. División Bioquímica Nuclear; ArgentinaFil: Juvenal, Guillermo Juan. Comision Nacional de Energía Atómica. Gerencia de Área de Aplicaciones de la Tecnología Nuclear. División Bioquímica Nuclear; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Pisarev, Mario Alberto. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; Argentina. Comision Nacional de Energía Atómica. Gerencia de Área de Aplicaciones de la Tecnología Nuclear. División Bioquímica Nuclear; ArgentinaMary Ann Liebert Inc2010-09info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/16264Thomasz, Lisa; Oglio, Andrea Romina; Randi, Andrea Silvana; Fernandez, Marina Olga; Dagrosa, Maria Alejandra; et al.; Biochemical changes during goiter induction by methylmercaptoimidazol and inhibition by δ-iodolactone in rat; Mary Ann Liebert Inc; Thyroid; 20; 9; 9-2010; 1003-10131050-7256enginfo:eu-repo/semantics/altIdentifier/doi/10.1089/thy.2009.0257info:eu-repo/semantics/altIdentifier/url/http://online.liebertpub.com/doi/pdf/10.1089/thy.2009.0257info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-10-15T14:39:06Zoai:ri.conicet.gov.ar:11336/16264instacron:CONICETInstitucionalhttp://ri.conicet.gov.ar/Organismo científico-tecnológicoNo correspondehttp://ri.conicet.gov.ar/oai/requestdasensio@conicet.gov.ar; lcarlino@conicet.gov.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:34982025-10-15 14:39:06.863CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Biochemical changes during goiter induction by methylmercaptoimidazol and inhibition by δ-iodolactone in rat
title Biochemical changes during goiter induction by methylmercaptoimidazol and inhibition by δ-iodolactone in rat
spellingShingle Biochemical changes during goiter induction by methylmercaptoimidazol and inhibition by δ-iodolactone in rat
Thomasz, Lisa
Thyroid
Iodolipid
Autorregulation
title_short Biochemical changes during goiter induction by methylmercaptoimidazol and inhibition by δ-iodolactone in rat
title_full Biochemical changes during goiter induction by methylmercaptoimidazol and inhibition by δ-iodolactone in rat
title_fullStr Biochemical changes during goiter induction by methylmercaptoimidazol and inhibition by δ-iodolactone in rat
title_full_unstemmed Biochemical changes during goiter induction by methylmercaptoimidazol and inhibition by δ-iodolactone in rat
title_sort Biochemical changes during goiter induction by methylmercaptoimidazol and inhibition by δ-iodolactone in rat
dc.creator.none.fl_str_mv Thomasz, Lisa
Oglio, Andrea Romina
Randi, Andrea Silvana
Fernandez, Marina Olga
Dagrosa, Maria Alejandra
Cabrini, Romulo L.
Juvenal, Guillermo Juan
Pisarev, Mario Alberto
author Thomasz, Lisa
author_facet Thomasz, Lisa
Oglio, Andrea Romina
Randi, Andrea Silvana
Fernandez, Marina Olga
Dagrosa, Maria Alejandra
Cabrini, Romulo L.
Juvenal, Guillermo Juan
Pisarev, Mario Alberto
author_role author
author2 Oglio, Andrea Romina
Randi, Andrea Silvana
Fernandez, Marina Olga
Dagrosa, Maria Alejandra
Cabrini, Romulo L.
Juvenal, Guillermo Juan
Pisarev, Mario Alberto
author2_role author
author
author
author
author
author
author
dc.subject.none.fl_str_mv Thyroid
Iodolipid
Autorregulation
topic Thyroid
Iodolipid
Autorregulation
purl_subject.fl_str_mv https://purl.org/becyt/ford/3.1
https://purl.org/becyt/ford/3
dc.description.none.fl_txt_mv Background: We have demonstrated that the administration of δ-iodolactone (i.e., 5-iodo-delta lactone) of arachidonic acid (IL-δ), a mediator in thyroid autoregulation, prevents goiter induction by methylmercaptoimidazol (MMI) in rats. Other studies have shown that transforming growth factor beta-1 (TGF-β1) mimics some of the actions of excess iodide, but its participation in autoregulation is disputed. The present studies were performed to test the hypotheses that IL-δ decreases thyroid growth by inhibition of cell proliferation and/or by stimulation of apoptosis due to oxidative stress, that TGF-β is stimulated by an excess of iodide and by IL-δ, and that c-Myc and c-Fos expression are upregulated during goiter induction and downregulated during goiter inhibition. Methods: Rats were treated with MMI alone or together with iodide or IL-δ. Thyroid weight, cell number, cell proliferation, apoptosis, and oxidative stress were determined. Proliferating cell nuclear antigen (PCNA), TGF-β1, TGF-β3, c-Myc, and c-Fos were measured by Western blot. Results: MMI caused a progressive increase in thyroid weight accompanied by an increase in cell number, asymmetry of the ploidy histograms, and PCNA, c-Fos, and c-Myc expression. In addition, an early increase of apoptosis was observed. Peroxides as well as glutathione peroxidase and catalase activities were also increased in goitrous animals. The inhibitory action of IL-δ on goiter formation was accompanied by the inhibition of cell proliferation evidenced by a significant decrease in cell number, PCNA expression, and asymmetry of the ploidy histograms. A transient stimulation of apoptosis after 7 days of treatment was also observed. MMI administration stimulated TGF-β1 but not TGF-β3 synthesis. IL-δ alone caused a slight increase of TGF-β3 but not TGF-β1, whereas potassium iodide (KI) stimulated both isoforms and MMI reversed KI effect on TGF-β1 expression but not on TGF-β3. Conclusions: The goiter inhibitory action of IL-δ is due to the inhibition of cell proliferation and the transient stimulation of apoptosis. This latter action does not involve oxidative stress. TGF-β1 does not play a role in the autoregulatory pathway mediated by IL-δ. Iodide stimulates TGF-β3 without the need of being organified. These results suggest that there may be more than one pathway involved in the autoregulatory mechanism.
Fil: Thomasz, Lisa. Comision Nacional de Energía Atómica. Gerencia de Área de Aplicaciones de la Tecnología Nuclear. División Bioquímica Nuclear; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Oglio, Andrea Romina. Comision Nacional de Energía Atómica. Gerencia de Área de Aplicaciones de la Tecnología Nuclear. División Bioquímica Nuclear; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Randi, Andrea Silvana. Universidad de Buenos Aires. Facultad de Medicina. Departamento de Bioquímica Humana; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Fernandez, Marina Olga. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Dagrosa, Maria Alejandra. Comision Nacional de Energía Atómica. Gerencia de Área de Aplicaciones de la Tecnología Nuclear. División Bioquímica Nuclear; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Cabrini, Romulo L.. Comision Nacional de Energía Atómica. Gerencia de Área de Aplicaciones de la Tecnología Nuclear. División Bioquímica Nuclear; Argentina
Fil: Juvenal, Guillermo Juan. Comision Nacional de Energía Atómica. Gerencia de Área de Aplicaciones de la Tecnología Nuclear. División Bioquímica Nuclear; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Pisarev, Mario Alberto. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; Argentina. Comision Nacional de Energía Atómica. Gerencia de Área de Aplicaciones de la Tecnología Nuclear. División Bioquímica Nuclear; Argentina
description Background: We have demonstrated that the administration of δ-iodolactone (i.e., 5-iodo-delta lactone) of arachidonic acid (IL-δ), a mediator in thyroid autoregulation, prevents goiter induction by methylmercaptoimidazol (MMI) in rats. Other studies have shown that transforming growth factor beta-1 (TGF-β1) mimics some of the actions of excess iodide, but its participation in autoregulation is disputed. The present studies were performed to test the hypotheses that IL-δ decreases thyroid growth by inhibition of cell proliferation and/or by stimulation of apoptosis due to oxidative stress, that TGF-β is stimulated by an excess of iodide and by IL-δ, and that c-Myc and c-Fos expression are upregulated during goiter induction and downregulated during goiter inhibition. Methods: Rats were treated with MMI alone or together with iodide or IL-δ. Thyroid weight, cell number, cell proliferation, apoptosis, and oxidative stress were determined. Proliferating cell nuclear antigen (PCNA), TGF-β1, TGF-β3, c-Myc, and c-Fos were measured by Western blot. Results: MMI caused a progressive increase in thyroid weight accompanied by an increase in cell number, asymmetry of the ploidy histograms, and PCNA, c-Fos, and c-Myc expression. In addition, an early increase of apoptosis was observed. Peroxides as well as glutathione peroxidase and catalase activities were also increased in goitrous animals. The inhibitory action of IL-δ on goiter formation was accompanied by the inhibition of cell proliferation evidenced by a significant decrease in cell number, PCNA expression, and asymmetry of the ploidy histograms. A transient stimulation of apoptosis after 7 days of treatment was also observed. MMI administration stimulated TGF-β1 but not TGF-β3 synthesis. IL-δ alone caused a slight increase of TGF-β3 but not TGF-β1, whereas potassium iodide (KI) stimulated both isoforms and MMI reversed KI effect on TGF-β1 expression but not on TGF-β3. Conclusions: The goiter inhibitory action of IL-δ is due to the inhibition of cell proliferation and the transient stimulation of apoptosis. This latter action does not involve oxidative stress. TGF-β1 does not play a role in the autoregulatory pathway mediated by IL-δ. Iodide stimulates TGF-β3 without the need of being organified. These results suggest that there may be more than one pathway involved in the autoregulatory mechanism.
publishDate 2010
dc.date.none.fl_str_mv 2010-09
dc.type.none.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
http://purl.org/coar/resource_type/c_6501
info:ar-repo/semantics/articulo
format article
status_str publishedVersion
dc.identifier.none.fl_str_mv http://hdl.handle.net/11336/16264
Thomasz, Lisa; Oglio, Andrea Romina; Randi, Andrea Silvana; Fernandez, Marina Olga; Dagrosa, Maria Alejandra; et al.; Biochemical changes during goiter induction by methylmercaptoimidazol and inhibition by δ-iodolactone in rat; Mary Ann Liebert Inc; Thyroid; 20; 9; 9-2010; 1003-1013
1050-7256
url http://hdl.handle.net/11336/16264
identifier_str_mv Thomasz, Lisa; Oglio, Andrea Romina; Randi, Andrea Silvana; Fernandez, Marina Olga; Dagrosa, Maria Alejandra; et al.; Biochemical changes during goiter induction by methylmercaptoimidazol and inhibition by δ-iodolactone in rat; Mary Ann Liebert Inc; Thyroid; 20; 9; 9-2010; 1003-1013
1050-7256
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/doi/10.1089/thy.2009.0257
info:eu-repo/semantics/altIdentifier/url/http://online.liebertpub.com/doi/pdf/10.1089/thy.2009.0257
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
eu_rights_str_mv openAccess
rights_invalid_str_mv https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
dc.format.none.fl_str_mv application/pdf
application/pdf
dc.publisher.none.fl_str_mv Mary Ann Liebert Inc
publisher.none.fl_str_mv Mary Ann Liebert Inc
dc.source.none.fl_str_mv reponame:CONICET Digital (CONICET)
instname:Consejo Nacional de Investigaciones Científicas y Técnicas
reponame_str CONICET Digital (CONICET)
collection CONICET Digital (CONICET)
instname_str Consejo Nacional de Investigaciones Científicas y Técnicas
repository.name.fl_str_mv CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicas
repository.mail.fl_str_mv dasensio@conicet.gov.ar; lcarlino@conicet.gov.ar
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score 13.22299

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