Reactive oxygen species sources and biomolecular oxidative damage induced by aflatoxin B1 and fumonisin B1 in rat spleen mononuclear cells

Autores
Mary, Verónica Sofía; Theumer, Martín Gustavo; Arias, Silvina Lorena; Rubinstein, Héctor Ramón
Año de publicación
2012
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
Aflatoxin B1 (AFB1) and fumonisin B1 (FB1) are mycotoxins widely found as cereal contaminants. Their immunotoxicities predispose to infectious diseases and may alter the tumor immune surveillance of human and animals, but the mechanisms underlying have not been fully elucidated, and the induction of oxidative stress has been proposed as a probable mechanism.This work was aimed at evaluating in spleen mononuclear cells (SMC) from Wistar rats the effects of the exposure, over cellular oxidative status, as well as at elucidating the contribution of different reactive oxygen species (ROS) to biomolecular oxidative damage, the biochemical pathways involved, and the probable interaction of both toxins to induce oxidative stress.All the treatments increased total ROS and oxidation of biomolecules, with MIX having the greatest effects. However, only MIX increased superoxide anion radical. The main ROS involved in oxidation of proteins, lipids and DNA appear to be hydrogen peroxide and hydroxyl radical. The mitochondrial complex I and CYP450 were involved in the ROS generation induced by all treatments. The NADPH oxidase system was induced by FB1 and MIX. The arachidonic acid metabolism contributed to the ROS formation induced by AFB1 and MIX. These results demonstrate that an interaction between AFB1 and FB1 occur in the oxidative stress induction, and show the biochemical pathways involved in ROS generation in SMC. The oxidative stress could mediate the AFB1 and FB1 individual and combined immunotoxicities.
Fil: Mary, Verónica Sofía. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Córdoba. Centro de Investigaciones en Bioquímica Clínica e Inmunología; Argentina
Fil: Theumer, Martín Gustavo. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Córdoba. Centro de Investigaciones en Bioquímica Clínica e Inmunología; Argentina
Fil: Arias, Silvina Lorena. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Córdoba. Centro de Investigaciones en Bioquímica Clínica e Inmunología; Argentina
Fil: Rubinstein, Héctor Ramón. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Córdoba. Centro de Investigaciones en Bioquímica Clínica e Inmunología; Argentina
Materia
Aflatoxin B1
Fumonisin B1
ROS sources
Biomolecular oxidative damage
Immunotoxicity
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:11336/273423
Acceder
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oai_identifier_str oai:ri.conicet.gov.ar:11336/273423
network_acronym_str CONICETDig
repository_id_str 3498
network_name_str CONICET Digital (CONICET)
spelling Reactive oxygen species sources and biomolecular oxidative damage induced by aflatoxin B1 and fumonisin B1 in rat spleen mononuclear cellsMary, Verónica SofíaTheumer, Martín GustavoArias, Silvina LorenaRubinstein, Héctor RamónAflatoxin B1Fumonisin B1ROS sourcesBiomolecular oxidative damageImmunotoxicityhttps://purl.org/becyt/ford/1.4https://purl.org/becyt/ford/1Aflatoxin B1 (AFB1) and fumonisin B1 (FB1) are mycotoxins widely found as cereal contaminants. Their immunotoxicities predispose to infectious diseases and may alter the tumor immune surveillance of human and animals, but the mechanisms underlying have not been fully elucidated, and the induction of oxidative stress has been proposed as a probable mechanism.This work was aimed at evaluating in spleen mononuclear cells (SMC) from Wistar rats the effects of the exposure, over cellular oxidative status, as well as at elucidating the contribution of different reactive oxygen species (ROS) to biomolecular oxidative damage, the biochemical pathways involved, and the probable interaction of both toxins to induce oxidative stress.All the treatments increased total ROS and oxidation of biomolecules, with MIX having the greatest effects. However, only MIX increased superoxide anion radical. The main ROS involved in oxidation of proteins, lipids and DNA appear to be hydrogen peroxide and hydroxyl radical. The mitochondrial complex I and CYP450 were involved in the ROS generation induced by all treatments. The NADPH oxidase system was induced by FB1 and MIX. The arachidonic acid metabolism contributed to the ROS formation induced by AFB1 and MIX. These results demonstrate that an interaction between AFB1 and FB1 occur in the oxidative stress induction, and show the biochemical pathways involved in ROS generation in SMC. The oxidative stress could mediate the AFB1 and FB1 individual and combined immunotoxicities.Fil: Mary, Verónica Sofía. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Córdoba. Centro de Investigaciones en Bioquímica Clínica e Inmunología; ArgentinaFil: Theumer, Martín Gustavo. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Córdoba. Centro de Investigaciones en Bioquímica Clínica e Inmunología; ArgentinaFil: Arias, Silvina Lorena. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Córdoba. Centro de Investigaciones en Bioquímica Clínica e Inmunología; ArgentinaFil: Rubinstein, Héctor Ramón. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Córdoba. Centro de Investigaciones en Bioquímica Clínica e Inmunología; ArgentinaElsevier Ireland2012-12info: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/11336/273423Mary, Verónica Sofía; Theumer, Martín Gustavo; Arias, Silvina Lorena; Rubinstein, Héctor Ramón; Reactive oxygen species sources and biomolecular oxidative damage induced by aflatoxin B1 and fumonisin B1 in rat spleen mononuclear cells; Elsevier Ireland; Toxicology; 302; 2-3; 12-2012; 299-3070300-483XCONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/url/http://www.sciencedirect.com/science/article/pii/S0300483X1200337Xinfo:eu-repo/semantics/altIdentifier/doi/10.1016/j.tox.2012.08.012info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-10-22T12:06:49Zoai:ri.conicet.gov.ar:11336/273423instacron: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 12:06:50.263CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Reactive oxygen species sources and biomolecular oxidative damage induced by aflatoxin B1 and fumonisin B1 in rat spleen mononuclear cells
title Reactive oxygen species sources and biomolecular oxidative damage induced by aflatoxin B1 and fumonisin B1 in rat spleen mononuclear cells
spellingShingle Reactive oxygen species sources and biomolecular oxidative damage induced by aflatoxin B1 and fumonisin B1 in rat spleen mononuclear cells
Mary, Verónica Sofía
Aflatoxin B1
Fumonisin B1
ROS sources
Biomolecular oxidative damage
Immunotoxicity
title_short Reactive oxygen species sources and biomolecular oxidative damage induced by aflatoxin B1 and fumonisin B1 in rat spleen mononuclear cells
title_full Reactive oxygen species sources and biomolecular oxidative damage induced by aflatoxin B1 and fumonisin B1 in rat spleen mononuclear cells
title_fullStr Reactive oxygen species sources and biomolecular oxidative damage induced by aflatoxin B1 and fumonisin B1 in rat spleen mononuclear cells
title_full_unstemmed Reactive oxygen species sources and biomolecular oxidative damage induced by aflatoxin B1 and fumonisin B1 in rat spleen mononuclear cells
title_sort Reactive oxygen species sources and biomolecular oxidative damage induced by aflatoxin B1 and fumonisin B1 in rat spleen mononuclear cells
dc.creator.none.fl_str_mv Mary, Verónica Sofía
Theumer, Martín Gustavo
Arias, Silvina Lorena
Rubinstein, Héctor Ramón
author Mary, Verónica Sofía
author_facet Mary, Verónica Sofía
Theumer, Martín Gustavo
Arias, Silvina Lorena
Rubinstein, Héctor Ramón
author_role author
author2 Theumer, Martín Gustavo
Arias, Silvina Lorena
Rubinstein, Héctor Ramón
author2_role author
author
author
dc.subject.none.fl_str_mv Aflatoxin B1
Fumonisin B1
ROS sources
Biomolecular oxidative damage
Immunotoxicity
topic Aflatoxin B1
Fumonisin B1
ROS sources
Biomolecular oxidative damage
Immunotoxicity
purl_subject.fl_str_mv https://purl.org/becyt/ford/1.4
https://purl.org/becyt/ford/1
dc.description.none.fl_txt_mv Aflatoxin B1 (AFB1) and fumonisin B1 (FB1) are mycotoxins widely found as cereal contaminants. Their immunotoxicities predispose to infectious diseases and may alter the tumor immune surveillance of human and animals, but the mechanisms underlying have not been fully elucidated, and the induction of oxidative stress has been proposed as a probable mechanism.This work was aimed at evaluating in spleen mononuclear cells (SMC) from Wistar rats the effects of the exposure, over cellular oxidative status, as well as at elucidating the contribution of different reactive oxygen species (ROS) to biomolecular oxidative damage, the biochemical pathways involved, and the probable interaction of both toxins to induce oxidative stress.All the treatments increased total ROS and oxidation of biomolecules, with MIX having the greatest effects. However, only MIX increased superoxide anion radical. The main ROS involved in oxidation of proteins, lipids and DNA appear to be hydrogen peroxide and hydroxyl radical. The mitochondrial complex I and CYP450 were involved in the ROS generation induced by all treatments. The NADPH oxidase system was induced by FB1 and MIX. The arachidonic acid metabolism contributed to the ROS formation induced by AFB1 and MIX. These results demonstrate that an interaction between AFB1 and FB1 occur in the oxidative stress induction, and show the biochemical pathways involved in ROS generation in SMC. The oxidative stress could mediate the AFB1 and FB1 individual and combined immunotoxicities.
Fil: Mary, Verónica Sofía. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Córdoba. Centro de Investigaciones en Bioquímica Clínica e Inmunología; Argentina
Fil: Theumer, Martín Gustavo. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Córdoba. Centro de Investigaciones en Bioquímica Clínica e Inmunología; Argentina
Fil: Arias, Silvina Lorena. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Córdoba. Centro de Investigaciones en Bioquímica Clínica e Inmunología; Argentina
Fil: Rubinstein, Héctor Ramón. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Córdoba. Centro de Investigaciones en Bioquímica Clínica e Inmunología; Argentina
description Aflatoxin B1 (AFB1) and fumonisin B1 (FB1) are mycotoxins widely found as cereal contaminants. Their immunotoxicities predispose to infectious diseases and may alter the tumor immune surveillance of human and animals, but the mechanisms underlying have not been fully elucidated, and the induction of oxidative stress has been proposed as a probable mechanism.This work was aimed at evaluating in spleen mononuclear cells (SMC) from Wistar rats the effects of the exposure, over cellular oxidative status, as well as at elucidating the contribution of different reactive oxygen species (ROS) to biomolecular oxidative damage, the biochemical pathways involved, and the probable interaction of both toxins to induce oxidative stress.All the treatments increased total ROS and oxidation of biomolecules, with MIX having the greatest effects. However, only MIX increased superoxide anion radical. The main ROS involved in oxidation of proteins, lipids and DNA appear to be hydrogen peroxide and hydroxyl radical. The mitochondrial complex I and CYP450 were involved in the ROS generation induced by all treatments. The NADPH oxidase system was induced by FB1 and MIX. The arachidonic acid metabolism contributed to the ROS formation induced by AFB1 and MIX. These results demonstrate that an interaction between AFB1 and FB1 occur in the oxidative stress induction, and show the biochemical pathways involved in ROS generation in SMC. The oxidative stress could mediate the AFB1 and FB1 individual and combined immunotoxicities.
publishDate 2012
dc.date.none.fl_str_mv 2012-12
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/11336/273423
Mary, Verónica Sofía; Theumer, Martín Gustavo; Arias, Silvina Lorena; Rubinstein, Héctor Ramón; Reactive oxygen species sources and biomolecular oxidative damage induced by aflatoxin B1 and fumonisin B1 in rat spleen mononuclear cells; Elsevier Ireland; Toxicology; 302; 2-3; 12-2012; 299-307
0300-483X
CONICET Digital
CONICET
url http://hdl.handle.net/11336/273423
identifier_str_mv Mary, Verónica Sofía; Theumer, Martín Gustavo; Arias, Silvina Lorena; Rubinstein, Héctor Ramón; Reactive oxygen species sources and biomolecular oxidative damage induced by aflatoxin B1 and fumonisin B1 in rat spleen mononuclear cells; Elsevier Ireland; Toxicology; 302; 2-3; 12-2012; 299-307
0300-483X
CONICET Digital
CONICET
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/url/http://www.sciencedirect.com/science/article/pii/S0300483X1200337X
info:eu-repo/semantics/altIdentifier/doi/10.1016/j.tox.2012.08.012
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
application/pdf
application/pdf
application/pdf
dc.publisher.none.fl_str_mv Elsevier Ireland
publisher.none.fl_str_mv Elsevier Ireland
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 12.982451

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