Foxo3 gene expression and oxidative status in beta-thalassemia minor subjects

Autores
Lazarte, Sandra Stella; Monaco, Maria Eugenia; Teran, Magdalena María; Haro, Ana Cecilia; Ledesma, Miryam Emilse; Isse, Blanca Alicia de Los Angeles G.
Año de publicación
2017
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
Background Oxidative stress may aggravate symptoms of hemolytic anemias such as beta-thalassemia. FoxO3 activation results in resistance to oxidative stress in fibroblasts and neuronal cell cultures. Objective The purpose of this research was to study FoxO3 gene expression and oxidative status in beta-thalassemia minor individuals. Methods Sixty-three subjects (42 apparently healthy individuals and 21 with beta-thalassemia minor) were analyzed at the Universidad Nacional de Tucumán, Argentina, between September 2013 and June 2014. A complete blood count, hemoglobin electrophoresis in alkaline pH and hemoglobin A2 levels were quantified. Moreover, thiobarbituric acid reactive species, erythrocyte catalase activity and iron status were evaluated. Beta-thalassemia mutations were determined by real-time polymerase chain reaction. FoxO3 gene expression was investigated by real-time reverse transcription-polymerase chain reaction using mononuclear cells from peripheral blood. Results Subjects were grouped as children (≤12 years), and adult women and men. The analysis of erythrocyte catalase activity/hemoglobin ratio revealed a significant difference (p-value <0.05) between healthy and beta-thalassemia minor adults, but no significant difference was observed in the thiobarbituric acid reactive species levels and FoxO3 gene expression (p-value >0.05). Thiobarbituric acid reactive species and the erythrocyte catalase activity/hemoglobin ratio were not significantly different on comparing the type of beta-thalassemia mutation (β0 or β+) present in carriers. Conclusions The lack of systemic oxidative imbalance demonstrated by thiobarbituric acid reactive species is correlated to the observation of normal FoxO3 gene expression in mononuclear cells of peripheral blood. However, an imbalanced antioxidant state was shown by the erythrocyte catalase activity/hemoglobin ratio in beta-thalassemia minor carriers. It would be necessary to study FoxO3 gene expression in reticulocytes to elucidate the role of FoxO3 in this pathology.
Fil: Lazarte, Sandra Stella. Universidad Nacional de Tucumán. Facultad de Bioquímica, Química y Farmacia; Argentina
Fil: Monaco, Maria Eugenia. Universidad Nacional de Tucumán. Facultad de Bioquímica, Química y Farmacia; Argentina
Fil: Teran, Magdalena María. Universidad Nacional de Tucumán. Facultad de Bioquímica, Química y Farmacia; Argentina
Fil: Haro, Ana Cecilia. Universidad Nacional de Tucumán. Facultad de Bioquímica, Química y Farmacia; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Tucumán; Argentina
Fil: Ledesma, Miryam Emilse. Universidad Nacional de Tucumán. Facultad de Bioquímica, Química y Farmacia; Argentina
Fil: Isse, Blanca Alicia de Los Angeles G.. Universidad Nacional de Tucumán. Facultad de Bioquímica, Química y Farmacia; Argentina
Materia
Beta-Thalassemia Trait
Erythrocyte Catalase Activity
Foxo3
Oxidative Stress
Thiobarbituric Acid Reactive Species
Nivel de accesibilidad
acceso abierto
Condiciones de uso
https://creativecommons.org/licenses/by-nc-nd/2.5/ar/
Repositorio
CONICET Digital (CONICET)
Institución
Consejo Nacional de Investigaciones Científicas y Técnicas
OAI Identificador
oai:ri.conicet.gov.ar:11336/67113
Acceder
id CONICETDig_114aacdbeef79511152bda3d7ae85e69
oai_identifier_str oai:ri.conicet.gov.ar:11336/67113
network_acronym_str CONICETDig
repository_id_str 3498
network_name_str CONICET Digital (CONICET)
spelling Foxo3 gene expression and oxidative status in beta-thalassemia minor subjectsLazarte, Sandra StellaMonaco, Maria EugeniaTeran, Magdalena MaríaHaro, Ana CeciliaLedesma, Miryam EmilseIsse, Blanca Alicia de Los Angeles G.Beta-Thalassemia TraitErythrocyte Catalase ActivityFoxo3Oxidative StressThiobarbituric Acid Reactive Specieshttps://purl.org/becyt/ford/3.3https://purl.org/becyt/ford/3Background Oxidative stress may aggravate symptoms of hemolytic anemias such as beta-thalassemia. FoxO3 activation results in resistance to oxidative stress in fibroblasts and neuronal cell cultures. Objective The purpose of this research was to study FoxO3 gene expression and oxidative status in beta-thalassemia minor individuals. Methods Sixty-three subjects (42 apparently healthy individuals and 21 with beta-thalassemia minor) were analyzed at the Universidad Nacional de Tucumán, Argentina, between September 2013 and June 2014. A complete blood count, hemoglobin electrophoresis in alkaline pH and hemoglobin A2 levels were quantified. Moreover, thiobarbituric acid reactive species, erythrocyte catalase activity and iron status were evaluated. Beta-thalassemia mutations were determined by real-time polymerase chain reaction. FoxO3 gene expression was investigated by real-time reverse transcription-polymerase chain reaction using mononuclear cells from peripheral blood. Results Subjects were grouped as children (≤12 years), and adult women and men. The analysis of erythrocyte catalase activity/hemoglobin ratio revealed a significant difference (p-value <0.05) between healthy and beta-thalassemia minor adults, but no significant difference was observed in the thiobarbituric acid reactive species levels and FoxO3 gene expression (p-value >0.05). Thiobarbituric acid reactive species and the erythrocyte catalase activity/hemoglobin ratio were not significantly different on comparing the type of beta-thalassemia mutation (β0 or β+) present in carriers. Conclusions The lack of systemic oxidative imbalance demonstrated by thiobarbituric acid reactive species is correlated to the observation of normal FoxO3 gene expression in mononuclear cells of peripheral blood. However, an imbalanced antioxidant state was shown by the erythrocyte catalase activity/hemoglobin ratio in beta-thalassemia minor carriers. It would be necessary to study FoxO3 gene expression in reticulocytes to elucidate the role of FoxO3 in this pathology.Fil: Lazarte, Sandra Stella. Universidad Nacional de Tucumán. Facultad de Bioquímica, Química y Farmacia; ArgentinaFil: Monaco, Maria Eugenia. Universidad Nacional de Tucumán. Facultad de Bioquímica, Química y Farmacia; ArgentinaFil: Teran, Magdalena María. Universidad Nacional de Tucumán. Facultad de Bioquímica, Química y Farmacia; ArgentinaFil: Haro, Ana Cecilia. Universidad Nacional de Tucumán. Facultad de Bioquímica, Química y Farmacia; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Tucumán; ArgentinaFil: Ledesma, Miryam Emilse. Universidad Nacional de Tucumán. Facultad de Bioquímica, Química y Farmacia; ArgentinaFil: Isse, Blanca Alicia de Los Angeles G.. Universidad Nacional de Tucumán. Facultad de Bioquímica, Química y Farmacia; ArgentinaAssociação Brasileira de Hematologia, Hemoterapia e Terapia Celular2017-04info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfapplication/pdfapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/67113Lazarte, Sandra Stella; Monaco, Maria Eugenia; Teran, Magdalena María; Haro, Ana Cecilia; Ledesma, Miryam Emilse; et al.; Foxo3 gene expression and oxidative status in beta-thalassemia minor subjects; Associação Brasileira de Hematologia, Hemoterapia e Terapia Celular; Revista Brasileira de Hematologia E Hemoterapia; 39; 2; 4-2017; 115-1211516-84841806-0870CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/url/https://www.sciencedirect.com/science/article/pii/S1516848417300270info:eu-repo/semantics/altIdentifier/doi/10.1016/j.bjhh.2017.01.005info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-nd/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-10-22T11:24:09Zoai:ri.conicet.gov.ar:11336/67113instacron: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 11:24:09.892CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Foxo3 gene expression and oxidative status in beta-thalassemia minor subjects
title Foxo3 gene expression and oxidative status in beta-thalassemia minor subjects
spellingShingle Foxo3 gene expression and oxidative status in beta-thalassemia minor subjects
Lazarte, Sandra Stella
Beta-Thalassemia Trait
Erythrocyte Catalase Activity
Foxo3
Oxidative Stress
Thiobarbituric Acid Reactive Species
title_short Foxo3 gene expression and oxidative status in beta-thalassemia minor subjects
title_full Foxo3 gene expression and oxidative status in beta-thalassemia minor subjects
title_fullStr Foxo3 gene expression and oxidative status in beta-thalassemia minor subjects
title_full_unstemmed Foxo3 gene expression and oxidative status in beta-thalassemia minor subjects
title_sort Foxo3 gene expression and oxidative status in beta-thalassemia minor subjects
dc.creator.none.fl_str_mv Lazarte, Sandra Stella
Monaco, Maria Eugenia
Teran, Magdalena María
Haro, Ana Cecilia
Ledesma, Miryam Emilse
Isse, Blanca Alicia de Los Angeles G.
author Lazarte, Sandra Stella
author_facet Lazarte, Sandra Stella
Monaco, Maria Eugenia
Teran, Magdalena María
Haro, Ana Cecilia
Ledesma, Miryam Emilse
Isse, Blanca Alicia de Los Angeles G.
author_role author
author2 Monaco, Maria Eugenia
Teran, Magdalena María
Haro, Ana Cecilia
Ledesma, Miryam Emilse
Isse, Blanca Alicia de Los Angeles G.
author2_role author
author
author
author
author
dc.subject.none.fl_str_mv Beta-Thalassemia Trait
Erythrocyte Catalase Activity
Foxo3
Oxidative Stress
Thiobarbituric Acid Reactive Species
topic Beta-Thalassemia Trait
Erythrocyte Catalase Activity
Foxo3
Oxidative Stress
Thiobarbituric Acid Reactive Species
purl_subject.fl_str_mv https://purl.org/becyt/ford/3.3
https://purl.org/becyt/ford/3
dc.description.none.fl_txt_mv Background Oxidative stress may aggravate symptoms of hemolytic anemias such as beta-thalassemia. FoxO3 activation results in resistance to oxidative stress in fibroblasts and neuronal cell cultures. Objective The purpose of this research was to study FoxO3 gene expression and oxidative status in beta-thalassemia minor individuals. Methods Sixty-three subjects (42 apparently healthy individuals and 21 with beta-thalassemia minor) were analyzed at the Universidad Nacional de Tucumán, Argentina, between September 2013 and June 2014. A complete blood count, hemoglobin electrophoresis in alkaline pH and hemoglobin A2 levels were quantified. Moreover, thiobarbituric acid reactive species, erythrocyte catalase activity and iron status were evaluated. Beta-thalassemia mutations were determined by real-time polymerase chain reaction. FoxO3 gene expression was investigated by real-time reverse transcription-polymerase chain reaction using mononuclear cells from peripheral blood. Results Subjects were grouped as children (≤12 years), and adult women and men. The analysis of erythrocyte catalase activity/hemoglobin ratio revealed a significant difference (p-value <0.05) between healthy and beta-thalassemia minor adults, but no significant difference was observed in the thiobarbituric acid reactive species levels and FoxO3 gene expression (p-value >0.05). Thiobarbituric acid reactive species and the erythrocyte catalase activity/hemoglobin ratio were not significantly different on comparing the type of beta-thalassemia mutation (β0 or β+) present in carriers. Conclusions The lack of systemic oxidative imbalance demonstrated by thiobarbituric acid reactive species is correlated to the observation of normal FoxO3 gene expression in mononuclear cells of peripheral blood. However, an imbalanced antioxidant state was shown by the erythrocyte catalase activity/hemoglobin ratio in beta-thalassemia minor carriers. It would be necessary to study FoxO3 gene expression in reticulocytes to elucidate the role of FoxO3 in this pathology.
Fil: Lazarte, Sandra Stella. Universidad Nacional de Tucumán. Facultad de Bioquímica, Química y Farmacia; Argentina
Fil: Monaco, Maria Eugenia. Universidad Nacional de Tucumán. Facultad de Bioquímica, Química y Farmacia; Argentina
Fil: Teran, Magdalena María. Universidad Nacional de Tucumán. Facultad de Bioquímica, Química y Farmacia; Argentina
Fil: Haro, Ana Cecilia. Universidad Nacional de Tucumán. Facultad de Bioquímica, Química y Farmacia; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Tucumán; Argentina
Fil: Ledesma, Miryam Emilse. Universidad Nacional de Tucumán. Facultad de Bioquímica, Química y Farmacia; Argentina
Fil: Isse, Blanca Alicia de Los Angeles G.. Universidad Nacional de Tucumán. Facultad de Bioquímica, Química y Farmacia; Argentina
description Background Oxidative stress may aggravate symptoms of hemolytic anemias such as beta-thalassemia. FoxO3 activation results in resistance to oxidative stress in fibroblasts and neuronal cell cultures. Objective The purpose of this research was to study FoxO3 gene expression and oxidative status in beta-thalassemia minor individuals. Methods Sixty-three subjects (42 apparently healthy individuals and 21 with beta-thalassemia minor) were analyzed at the Universidad Nacional de Tucumán, Argentina, between September 2013 and June 2014. A complete blood count, hemoglobin electrophoresis in alkaline pH and hemoglobin A2 levels were quantified. Moreover, thiobarbituric acid reactive species, erythrocyte catalase activity and iron status were evaluated. Beta-thalassemia mutations were determined by real-time polymerase chain reaction. FoxO3 gene expression was investigated by real-time reverse transcription-polymerase chain reaction using mononuclear cells from peripheral blood. Results Subjects were grouped as children (≤12 years), and adult women and men. The analysis of erythrocyte catalase activity/hemoglobin ratio revealed a significant difference (p-value <0.05) between healthy and beta-thalassemia minor adults, but no significant difference was observed in the thiobarbituric acid reactive species levels and FoxO3 gene expression (p-value >0.05). Thiobarbituric acid reactive species and the erythrocyte catalase activity/hemoglobin ratio were not significantly different on comparing the type of beta-thalassemia mutation (β0 or β+) present in carriers. Conclusions The lack of systemic oxidative imbalance demonstrated by thiobarbituric acid reactive species is correlated to the observation of normal FoxO3 gene expression in mononuclear cells of peripheral blood. However, an imbalanced antioxidant state was shown by the erythrocyte catalase activity/hemoglobin ratio in beta-thalassemia minor carriers. It would be necessary to study FoxO3 gene expression in reticulocytes to elucidate the role of FoxO3 in this pathology.
publishDate 2017
dc.date.none.fl_str_mv 2017-04
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/11336/67113
Lazarte, Sandra Stella; Monaco, Maria Eugenia; Teran, Magdalena María; Haro, Ana Cecilia; Ledesma, Miryam Emilse; et al.; Foxo3 gene expression and oxidative status in beta-thalassemia minor subjects; Associação Brasileira de Hematologia, Hemoterapia e Terapia Celular; Revista Brasileira de Hematologia E Hemoterapia; 39; 2; 4-2017; 115-121
1516-8484
1806-0870
CONICET Digital
CONICET
url http://hdl.handle.net/11336/67113
identifier_str_mv Lazarte, Sandra Stella; Monaco, Maria Eugenia; Teran, Magdalena María; Haro, Ana Cecilia; Ledesma, Miryam Emilse; et al.; Foxo3 gene expression and oxidative status in beta-thalassemia minor subjects; Associação Brasileira de Hematologia, Hemoterapia e Terapia Celular; Revista Brasileira de Hematologia E Hemoterapia; 39; 2; 4-2017; 115-121
1516-8484
1806-0870
CONICET Digital
CONICET
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/url/https://www.sciencedirect.com/science/article/pii/S1516848417300270
info:eu-repo/semantics/altIdentifier/doi/10.1016/j.bjhh.2017.01.005
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
https://creativecommons.org/licenses/by-nc-nd/2.5/ar/
eu_rights_str_mv openAccess
rights_invalid_str_mv https://creativecommons.org/licenses/by-nc-nd/2.5/ar/
dc.format.none.fl_str_mv application/pdf
application/pdf
application/pdf
application/pdf
application/pdf
dc.publisher.none.fl_str_mv Associação Brasileira de Hematologia, Hemoterapia e Terapia Celular
publisher.none.fl_str_mv Associação Brasileira de Hematologia, Hemoterapia e Terapia Celular
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
_version_ 1846781776780853248
score 12.982451

Publicaciones similares