Mitochondrial dysfunction in skeletal muscle during experimental Chagas disease

Autores
Báez, Alejandra Lidia; Reynoso, Mercedes María Noel; Lo Presti, Maria Silvina; Bazán, Paola Carolina; Strauss, Mariana; Miler, Noemí del Carmen; Pons, Patricia; Rivarola, Hector Walter; Paglini, Patricia Adriana
Año de publicación
2015
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
Trypanosoma cruzi invasion and replication in cardiomyocytes and other tissues induce cellular injuries and cytotoxic reactions, with the production of inflammatory cytokines and nitric oxide, both sources of reactive oxygen species. The myocyte response to oxidative stress involves the progression of cellular changes primarily targeting mitochondria. Similar alterations could be taking place in mitochondria from the skeletal muscle; if that is the case, a simple skeletal muscle biopsy would give information about the cardiac energetic production that could be used as a predictor of the chagasic cardiopathy evolution. Therefore, in the present paper we studied skeletal muscle mitochondrial structure and the enzymatic activity of citrate synthase and respiratory chain complexes I to IV (CI–CIV), in Albino Swiss mice infected with T. cruzi, Tulahuen strain and SGO Z12 and Lucky isolates, along the infection. Changes in the mitochondrial structure were detected in 100% of the mitochondria analyzed from the infected groups: they all presented at least 1 significant abnormality such as increase in their matrix or disorganization of their cristae, which are probably related to the enzymatic dysfunction. When we studied the Krebs cycle functionality through the measurement of the specific citrate synthase activity, we found it to be significantly diminished during the acute phase of the infection in Tulahuen and SGO Z12 infected groups with respect to the control one; citrate synthase activity from the Lucky group was significantly increased (p b 0.05). The activity of this enzyme was reduced in all the infected groups during the chronic asymptomatic phase (p b 0.001) and return to normal values (Tulahuen and SGO Z12) or increased its activity (Lucky) by day 365 post-infection (p.i.). When the mitochondrial respiratory chain was analyzed from the acute to the chronic phase of the infection through the measurement of the activity of complexes I to IV, the activity of CI remained similar to control in Tulahuen and Lucky groups, but was significantly augmented in the SGO Z12 one in the acute and chronic phases (p b 0.05). CII increased its activity in Tulahuen and Lucky groups by day 75 p.i. and in SGO Z12 by day 365 p.i. (p b 0.05). CIII showed a similar behavior in the 3 infected groups, remaining similar to control values in the first two stages of the infection and significantly increasing later on (p b 0.0001). CIV showed an increase in its activity in Lucky throughout all stages of infection (p b 0.0001) and an increase in Tulahuen by day 365 days p.i. (p b 0.0001); SGO Z12 on the other hand, showed a decreased CIV activity at the same time. The structural changes in skeletal muscle mitochondria and their altered enzyme activity began in the acute phase of infection, probably modifying the ability of mitochondria to generate energy; these changes were not compensated in the rest of the phases of the infection. Chagas is a systemic disease, which produces not only heart damage but also permanent skeletal muscle alterations.
Fil: Báez, Alejandra Lidia. Universidad Nacional de Córdoba. Facultad de Medicina. Departamento de Fisiología Humana y Física Biomedica; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba. Instituto de Investigaciones en Ciencias de la Salud. Universidad Nacional de Córdoba. Instituto de Investigaciones en Ciencias de la Salud; Argentina
Fil: Reynoso, Mercedes María Noel. Universidad Nacional de Córdoba. Facultad de Medicina. Departamento de Fisiología Humana y Física Biomedica; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba. Instituto de Investigaciones en Ciencias de la Salud. Universidad Nacional de Córdoba. Instituto de Investigaciones en Ciencias de la Salud; Argentina
Fil: Lo Presti, Maria Silvina. Universidad Nacional de Córdoba. Facultad de Medicina. Departamento de Fisiología Humana y Física Biomedica; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba. Instituto de Investigaciones en Ciencias de la Salud. Universidad Nacional de Córdoba. Instituto de Investigaciones en Ciencias de la Salud; Argentina
Fil: Bazán, Paola Carolina. Universidad Nacional de Córdoba. Facultad de Medicina. Departamento de Fisiología Humana y Física Biomedica; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba. Instituto de Investigaciones en Ciencias de la Salud. Universidad Nacional de Córdoba. Instituto de Investigaciones en Ciencias de la Salud; Argentina
Fil: Strauss, Mariana. Universidad Nacional de Córdoba. Facultad de Medicina. Departamento de Fisiología Humana y Física Biomedica; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba. Instituto de Investigaciones en Ciencias de la Salud. Universidad Nacional de Córdoba. Instituto de Investigaciones en Ciencias de la Salud; Argentina
Fil: Miler, Noemí del Carmen. Universidad Nacional de Córdoba. Facultad de Medicina. Departamento de Fisiología Humana y Física Biomedica; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba. Instituto de Investigaciones en Ciencias de la Salud. Universidad Nacional de Córdoba. Instituto de Investigaciones en Ciencias de la Salud; Argentina
Fil: Pons, Patricia. Universidad Nacional de Córdoba. Facultad de Medicina. Centro de Microscopía Electrónica; Argentina
Fil: Rivarola, Hector Walter. Universidad Nacional de Córdoba. Facultad de Medicina. Departamento de Fisiología Humana y Física Biomedica; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba. Instituto de Investigaciones en Ciencias de la Salud. Universidad Nacional de Córdoba. Instituto de Investigaciones en Ciencias de la Salud; Argentina
Fil: Paglini, Patricia Adriana. Universidad Nacional de Córdoba. Facultad de Medicina. Departamento de Fisiología Humana y Física Biomedica; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba. Instituto de Investigaciones en Ciencias de la Salud. Universidad Nacional de Córdoba. Instituto de Investigaciones en Ciencias de la Salud; Argentina
Materia
CHAGAS' DISEASE
KREBS CYCLE
MITOCHONDRIA
RESPIRATORY CHAIN
SKELETAL MUSCLE
TRYPANOSOMA CRUZI
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:11336/185629
Acceder
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spelling Mitochondrial dysfunction in skeletal muscle during experimental Chagas diseaseBáez, Alejandra LidiaReynoso, Mercedes María NoelLo Presti, Maria SilvinaBazán, Paola CarolinaStrauss, MarianaMiler, Noemí del CarmenPons, PatriciaRivarola, Hector WalterPaglini, Patricia AdrianaCHAGAS' DISEASEKREBS CYCLEMITOCHONDRIARESPIRATORY CHAINSKELETAL MUSCLETRYPANOSOMA CRUZIhttps://purl.org/becyt/ford/3.3https://purl.org/becyt/ford/3Trypanosoma cruzi invasion and replication in cardiomyocytes and other tissues induce cellular injuries and cytotoxic reactions, with the production of inflammatory cytokines and nitric oxide, both sources of reactive oxygen species. The myocyte response to oxidative stress involves the progression of cellular changes primarily targeting mitochondria. Similar alterations could be taking place in mitochondria from the skeletal muscle; if that is the case, a simple skeletal muscle biopsy would give information about the cardiac energetic production that could be used as a predictor of the chagasic cardiopathy evolution. Therefore, in the present paper we studied skeletal muscle mitochondrial structure and the enzymatic activity of citrate synthase and respiratory chain complexes I to IV (CI–CIV), in Albino Swiss mice infected with T. cruzi, Tulahuen strain and SGO Z12 and Lucky isolates, along the infection. Changes in the mitochondrial structure were detected in 100% of the mitochondria analyzed from the infected groups: they all presented at least 1 significant abnormality such as increase in their matrix or disorganization of their cristae, which are probably related to the enzymatic dysfunction. When we studied the Krebs cycle functionality through the measurement of the specific citrate synthase activity, we found it to be significantly diminished during the acute phase of the infection in Tulahuen and SGO Z12 infected groups with respect to the control one; citrate synthase activity from the Lucky group was significantly increased (p b 0.05). The activity of this enzyme was reduced in all the infected groups during the chronic asymptomatic phase (p b 0.001) and return to normal values (Tulahuen and SGO Z12) or increased its activity (Lucky) by day 365 post-infection (p.i.). When the mitochondrial respiratory chain was analyzed from the acute to the chronic phase of the infection through the measurement of the activity of complexes I to IV, the activity of CI remained similar to control in Tulahuen and Lucky groups, but was significantly augmented in the SGO Z12 one in the acute and chronic phases (p b 0.05). CII increased its activity in Tulahuen and Lucky groups by day 75 p.i. and in SGO Z12 by day 365 p.i. (p b 0.05). CIII showed a similar behavior in the 3 infected groups, remaining similar to control values in the first two stages of the infection and significantly increasing later on (p b 0.0001). CIV showed an increase in its activity in Lucky throughout all stages of infection (p b 0.0001) and an increase in Tulahuen by day 365 days p.i. (p b 0.0001); SGO Z12 on the other hand, showed a decreased CIV activity at the same time. The structural changes in skeletal muscle mitochondria and their altered enzyme activity began in the acute phase of infection, probably modifying the ability of mitochondria to generate energy; these changes were not compensated in the rest of the phases of the infection. Chagas is a systemic disease, which produces not only heart damage but also permanent skeletal muscle alterations.Fil: Báez, Alejandra Lidia. Universidad Nacional de Córdoba. Facultad de Medicina. Departamento de Fisiología Humana y Física Biomedica; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba. Instituto de Investigaciones en Ciencias de la Salud. Universidad Nacional de Córdoba. Instituto de Investigaciones en Ciencias de la Salud; ArgentinaFil: Reynoso, Mercedes María Noel. Universidad Nacional de Córdoba. Facultad de Medicina. Departamento de Fisiología Humana y Física Biomedica; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba. Instituto de Investigaciones en Ciencias de la Salud. Universidad Nacional de Córdoba. Instituto de Investigaciones en Ciencias de la Salud; ArgentinaFil: Lo Presti, Maria Silvina. Universidad Nacional de Córdoba. Facultad de Medicina. Departamento de Fisiología Humana y Física Biomedica; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba. Instituto de Investigaciones en Ciencias de la Salud. Universidad Nacional de Córdoba. Instituto de Investigaciones en Ciencias de la Salud; ArgentinaFil: Bazán, Paola Carolina. Universidad Nacional de Córdoba. Facultad de Medicina. Departamento de Fisiología Humana y Física Biomedica; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba. Instituto de Investigaciones en Ciencias de la Salud. Universidad Nacional de Córdoba. Instituto de Investigaciones en Ciencias de la Salud; ArgentinaFil: Strauss, Mariana. Universidad Nacional de Córdoba. Facultad de Medicina. Departamento de Fisiología Humana y Física Biomedica; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba. Instituto de Investigaciones en Ciencias de la Salud. Universidad Nacional de Córdoba. Instituto de Investigaciones en Ciencias de la Salud; ArgentinaFil: Miler, Noemí del Carmen. Universidad Nacional de Córdoba. Facultad de Medicina. Departamento de Fisiología Humana y Física Biomedica; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba. Instituto de Investigaciones en Ciencias de la Salud. Universidad Nacional de Córdoba. Instituto de Investigaciones en Ciencias de la Salud; ArgentinaFil: Pons, Patricia. Universidad Nacional de Córdoba. Facultad de Medicina. Centro de Microscopía Electrónica; ArgentinaFil: Rivarola, Hector Walter. Universidad Nacional de Córdoba. Facultad de Medicina. Departamento de Fisiología Humana y Física Biomedica; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba. Instituto de Investigaciones en Ciencias de la Salud. Universidad Nacional de Córdoba. Instituto de Investigaciones en Ciencias de la Salud; ArgentinaFil: Paglini, Patricia Adriana. Universidad Nacional de Córdoba. Facultad de Medicina. Departamento de Fisiología Humana y Física Biomedica; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba. Instituto de Investigaciones en Ciencias de la Salud. Universidad Nacional de Córdoba. Instituto de Investigaciones en Ciencias de la Salud; ArgentinaAcademic Press Inc Elsevier Science2015-06info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfapplication/pdfapplication/pdfapplication/pdfapplication/pdfapplication/pdfapplication/pdfapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/185629Báez, Alejandra Lidia; Reynoso, Mercedes María Noel; Lo Presti, Maria Silvina; Bazán, Paola Carolina; Strauss, Mariana; et al.; Mitochondrial dysfunction in skeletal muscle during experimental Chagas disease; Academic Press Inc Elsevier Science; Experimental and Molecular Pathology; 98; 3; 6-2015; 467-4750014-48001096-0945CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/url/https://www.sciencedirect.com/science/article/pii/S0014480015000696info:eu-repo/semantics/altIdentifier/doi/ 10.1016/j.yexmp.2015.03.034info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-10-22T11:22:17Zoai:ri.conicet.gov.ar:11336/185629instacron: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:34982025-10-22 11:22:17.771CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Mitochondrial dysfunction in skeletal muscle during experimental Chagas disease
title Mitochondrial dysfunction in skeletal muscle during experimental Chagas disease
spellingShingle Mitochondrial dysfunction in skeletal muscle during experimental Chagas disease
Báez, Alejandra Lidia
CHAGAS' DISEASE
KREBS CYCLE
MITOCHONDRIA
RESPIRATORY CHAIN
SKELETAL MUSCLE
TRYPANOSOMA CRUZI
title_short Mitochondrial dysfunction in skeletal muscle during experimental Chagas disease
title_full Mitochondrial dysfunction in skeletal muscle during experimental Chagas disease
title_fullStr Mitochondrial dysfunction in skeletal muscle during experimental Chagas disease
title_full_unstemmed Mitochondrial dysfunction in skeletal muscle during experimental Chagas disease
title_sort Mitochondrial dysfunction in skeletal muscle during experimental Chagas disease
dc.creator.none.fl_str_mv Báez, Alejandra Lidia
Reynoso, Mercedes María Noel
Lo Presti, Maria Silvina
Bazán, Paola Carolina
Strauss, Mariana
Miler, Noemí del Carmen
Pons, Patricia
Rivarola, Hector Walter
Paglini, Patricia Adriana
author Báez, Alejandra Lidia
author_facet Báez, Alejandra Lidia
Reynoso, Mercedes María Noel
Lo Presti, Maria Silvina
Bazán, Paola Carolina
Strauss, Mariana
Miler, Noemí del Carmen
Pons, Patricia
Rivarola, Hector Walter
Paglini, Patricia Adriana
author_role author
author2 Reynoso, Mercedes María Noel
Lo Presti, Maria Silvina
Bazán, Paola Carolina
Strauss, Mariana
Miler, Noemí del Carmen
Pons, Patricia
Rivarola, Hector Walter
Paglini, Patricia Adriana
author2_role author
author
author
author
author
author
author
author
dc.subject.none.fl_str_mv CHAGAS' DISEASE
KREBS CYCLE
MITOCHONDRIA
RESPIRATORY CHAIN
SKELETAL MUSCLE
TRYPANOSOMA CRUZI
topic CHAGAS' DISEASE
KREBS CYCLE
MITOCHONDRIA
RESPIRATORY CHAIN
SKELETAL MUSCLE
TRYPANOSOMA CRUZI
purl_subject.fl_str_mv https://purl.org/becyt/ford/3.3
https://purl.org/becyt/ford/3
dc.description.none.fl_txt_mv Trypanosoma cruzi invasion and replication in cardiomyocytes and other tissues induce cellular injuries and cytotoxic reactions, with the production of inflammatory cytokines and nitric oxide, both sources of reactive oxygen species. The myocyte response to oxidative stress involves the progression of cellular changes primarily targeting mitochondria. Similar alterations could be taking place in mitochondria from the skeletal muscle; if that is the case, a simple skeletal muscle biopsy would give information about the cardiac energetic production that could be used as a predictor of the chagasic cardiopathy evolution. Therefore, in the present paper we studied skeletal muscle mitochondrial structure and the enzymatic activity of citrate synthase and respiratory chain complexes I to IV (CI–CIV), in Albino Swiss mice infected with T. cruzi, Tulahuen strain and SGO Z12 and Lucky isolates, along the infection. Changes in the mitochondrial structure were detected in 100% of the mitochondria analyzed from the infected groups: they all presented at least 1 significant abnormality such as increase in their matrix or disorganization of their cristae, which are probably related to the enzymatic dysfunction. When we studied the Krebs cycle functionality through the measurement of the specific citrate synthase activity, we found it to be significantly diminished during the acute phase of the infection in Tulahuen and SGO Z12 infected groups with respect to the control one; citrate synthase activity from the Lucky group was significantly increased (p b 0.05). The activity of this enzyme was reduced in all the infected groups during the chronic asymptomatic phase (p b 0.001) and return to normal values (Tulahuen and SGO Z12) or increased its activity (Lucky) by day 365 post-infection (p.i.). When the mitochondrial respiratory chain was analyzed from the acute to the chronic phase of the infection through the measurement of the activity of complexes I to IV, the activity of CI remained similar to control in Tulahuen and Lucky groups, but was significantly augmented in the SGO Z12 one in the acute and chronic phases (p b 0.05). CII increased its activity in Tulahuen and Lucky groups by day 75 p.i. and in SGO Z12 by day 365 p.i. (p b 0.05). CIII showed a similar behavior in the 3 infected groups, remaining similar to control values in the first two stages of the infection and significantly increasing later on (p b 0.0001). CIV showed an increase in its activity in Lucky throughout all stages of infection (p b 0.0001) and an increase in Tulahuen by day 365 days p.i. (p b 0.0001); SGO Z12 on the other hand, showed a decreased CIV activity at the same time. The structural changes in skeletal muscle mitochondria and their altered enzyme activity began in the acute phase of infection, probably modifying the ability of mitochondria to generate energy; these changes were not compensated in the rest of the phases of the infection. Chagas is a systemic disease, which produces not only heart damage but also permanent skeletal muscle alterations.
Fil: Báez, Alejandra Lidia. Universidad Nacional de Córdoba. Facultad de Medicina. Departamento de Fisiología Humana y Física Biomedica; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba. Instituto de Investigaciones en Ciencias de la Salud. Universidad Nacional de Córdoba. Instituto de Investigaciones en Ciencias de la Salud; Argentina
Fil: Reynoso, Mercedes María Noel. Universidad Nacional de Córdoba. Facultad de Medicina. Departamento de Fisiología Humana y Física Biomedica; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba. Instituto de Investigaciones en Ciencias de la Salud. Universidad Nacional de Córdoba. Instituto de Investigaciones en Ciencias de la Salud; Argentina
Fil: Lo Presti, Maria Silvina. Universidad Nacional de Córdoba. Facultad de Medicina. Departamento de Fisiología Humana y Física Biomedica; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba. Instituto de Investigaciones en Ciencias de la Salud. Universidad Nacional de Córdoba. Instituto de Investigaciones en Ciencias de la Salud; Argentina
Fil: Bazán, Paola Carolina. Universidad Nacional de Córdoba. Facultad de Medicina. Departamento de Fisiología Humana y Física Biomedica; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba. Instituto de Investigaciones en Ciencias de la Salud. Universidad Nacional de Córdoba. Instituto de Investigaciones en Ciencias de la Salud; Argentina
Fil: Strauss, Mariana. Universidad Nacional de Córdoba. Facultad de Medicina. Departamento de Fisiología Humana y Física Biomedica; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba. Instituto de Investigaciones en Ciencias de la Salud. Universidad Nacional de Córdoba. Instituto de Investigaciones en Ciencias de la Salud; Argentina
Fil: Miler, Noemí del Carmen. Universidad Nacional de Córdoba. Facultad de Medicina. Departamento de Fisiología Humana y Física Biomedica; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba. Instituto de Investigaciones en Ciencias de la Salud. Universidad Nacional de Córdoba. Instituto de Investigaciones en Ciencias de la Salud; Argentina
Fil: Pons, Patricia. Universidad Nacional de Córdoba. Facultad de Medicina. Centro de Microscopía Electrónica; Argentina
Fil: Rivarola, Hector Walter. Universidad Nacional de Córdoba. Facultad de Medicina. Departamento de Fisiología Humana y Física Biomedica; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba. Instituto de Investigaciones en Ciencias de la Salud. Universidad Nacional de Córdoba. Instituto de Investigaciones en Ciencias de la Salud; Argentina
Fil: Paglini, Patricia Adriana. Universidad Nacional de Córdoba. Facultad de Medicina. Departamento de Fisiología Humana y Física Biomedica; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba. Instituto de Investigaciones en Ciencias de la Salud. Universidad Nacional de Córdoba. Instituto de Investigaciones en Ciencias de la Salud; Argentina
description Trypanosoma cruzi invasion and replication in cardiomyocytes and other tissues induce cellular injuries and cytotoxic reactions, with the production of inflammatory cytokines and nitric oxide, both sources of reactive oxygen species. The myocyte response to oxidative stress involves the progression of cellular changes primarily targeting mitochondria. Similar alterations could be taking place in mitochondria from the skeletal muscle; if that is the case, a simple skeletal muscle biopsy would give information about the cardiac energetic production that could be used as a predictor of the chagasic cardiopathy evolution. Therefore, in the present paper we studied skeletal muscle mitochondrial structure and the enzymatic activity of citrate synthase and respiratory chain complexes I to IV (CI–CIV), in Albino Swiss mice infected with T. cruzi, Tulahuen strain and SGO Z12 and Lucky isolates, along the infection. Changes in the mitochondrial structure were detected in 100% of the mitochondria analyzed from the infected groups: they all presented at least 1 significant abnormality such as increase in their matrix or disorganization of their cristae, which are probably related to the enzymatic dysfunction. When we studied the Krebs cycle functionality through the measurement of the specific citrate synthase activity, we found it to be significantly diminished during the acute phase of the infection in Tulahuen and SGO Z12 infected groups with respect to the control one; citrate synthase activity from the Lucky group was significantly increased (p b 0.05). The activity of this enzyme was reduced in all the infected groups during the chronic asymptomatic phase (p b 0.001) and return to normal values (Tulahuen and SGO Z12) or increased its activity (Lucky) by day 365 post-infection (p.i.). When the mitochondrial respiratory chain was analyzed from the acute to the chronic phase of the infection through the measurement of the activity of complexes I to IV, the activity of CI remained similar to control in Tulahuen and Lucky groups, but was significantly augmented in the SGO Z12 one in the acute and chronic phases (p b 0.05). CII increased its activity in Tulahuen and Lucky groups by day 75 p.i. and in SGO Z12 by day 365 p.i. (p b 0.05). CIII showed a similar behavior in the 3 infected groups, remaining similar to control values in the first two stages of the infection and significantly increasing later on (p b 0.0001). CIV showed an increase in its activity in Lucky throughout all stages of infection (p b 0.0001) and an increase in Tulahuen by day 365 days p.i. (p b 0.0001); SGO Z12 on the other hand, showed a decreased CIV activity at the same time. The structural changes in skeletal muscle mitochondria and their altered enzyme activity began in the acute phase of infection, probably modifying the ability of mitochondria to generate energy; these changes were not compensated in the rest of the phases of the infection. Chagas is a systemic disease, which produces not only heart damage but also permanent skeletal muscle alterations.
publishDate 2015
dc.date.none.fl_str_mv 2015-06
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/11336/185629
Báez, Alejandra Lidia; Reynoso, Mercedes María Noel; Lo Presti, Maria Silvina; Bazán, Paola Carolina; Strauss, Mariana; et al.; Mitochondrial dysfunction in skeletal muscle during experimental Chagas disease; Academic Press Inc Elsevier Science; Experimental and Molecular Pathology; 98; 3; 6-2015; 467-475
0014-4800
1096-0945
CONICET Digital
CONICET
url http://hdl.handle.net/11336/185629
identifier_str_mv Báez, Alejandra Lidia; Reynoso, Mercedes María Noel; Lo Presti, Maria Silvina; Bazán, Paola Carolina; Strauss, Mariana; et al.; Mitochondrial dysfunction in skeletal muscle during experimental Chagas disease; Academic Press Inc Elsevier Science; Experimental and Molecular Pathology; 98; 3; 6-2015; 467-475
0014-4800
1096-0945
CONICET Digital
CONICET
dc.language.none.fl_str_mv eng
language eng
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info:eu-repo/semantics/altIdentifier/doi/ 10.1016/j.yexmp.2015.03.034
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/
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dc.publisher.none.fl_str_mv Academic Press Inc Elsevier Science
publisher.none.fl_str_mv Academic Press Inc Elsevier Science
dc.source.none.fl_str_mv reponame:CONICET Digital (CONICET)
instname:Consejo Nacional de Investigaciones Científicas y Técnicas
reponame_str CONICET Digital (CONICET)
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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 12.8982525

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