High susceptibility of activated lymphocytes to oxidative stress-induced cell death
Autor(a) principal: | |
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Data de Publicação: | 2008 |
Outros Autores: | , |
Tipo de documento: | Artigo |
Idioma: | eng |
Título da fonte: | Anais da Academia Brasileira de Ciências (Online) |
Texto Completo: | http://old.scielo.br/scielo.php?script=sci_arttext&pid=S0001-37652008000100009 |
Resumo: | The present study provides evidence that activated spleen lymphocytes from Walker 256 tumor bearing rats are more susceptible than controls to tert-butyl hydroperoxide (t-BOOH)-induced necrotic cell death in vitro. The iron chelator and antioxidant deferoxamine, the intracellular Ca2+ chelator BAPTA, the L-type Ca2+ channel antagonist nifedipine or the mitochondrial permeability transition inhibitor cyclosporin A, but not the calcineurin inhibitor FK-506, render control and activated lymphocytes equally resistant to the toxic effects of t-BOOH. Incubation of activated lymphocytes in the presence of t-BOOH resulted in a cyclosporin A-sensitive decrease in mitochondrial membrane potential. These results indicate that the higher cytosolic Ca2+ level in activated lymphocytes increases their susceptibility to oxidative stress-induced cell death in a mechanism involving the participation of mitochondrial permeability transition. |
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Anais da Academia Brasileira de Ciências (Online) |
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High susceptibility of activated lymphocytes to oxidative stress-induced cell deathcell deathfree radicalsimmune responselymphopeniamitochondrial permeability transitionspleen lymphocyteThe present study provides evidence that activated spleen lymphocytes from Walker 256 tumor bearing rats are more susceptible than controls to tert-butyl hydroperoxide (t-BOOH)-induced necrotic cell death in vitro. The iron chelator and antioxidant deferoxamine, the intracellular Ca2+ chelator BAPTA, the L-type Ca2+ channel antagonist nifedipine or the mitochondrial permeability transition inhibitor cyclosporin A, but not the calcineurin inhibitor FK-506, render control and activated lymphocytes equally resistant to the toxic effects of t-BOOH. Incubation of activated lymphocytes in the presence of t-BOOH resulted in a cyclosporin A-sensitive decrease in mitochondrial membrane potential. These results indicate that the higher cytosolic Ca2+ level in activated lymphocytes increases their susceptibility to oxidative stress-induced cell death in a mechanism involving the participation of mitochondrial permeability transition.Academia Brasileira de Ciências2008-03-01info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersiontext/htmlhttp://old.scielo.br/scielo.php?script=sci_arttext&pid=S0001-37652008000100009Anais da Academia Brasileira de Ciências v.80 n.1 2008reponame:Anais da Academia Brasileira de Ciências (Online)instname:Academia Brasileira de Ciências (ABC)instacron:ABC10.1590/S0001-37652008000100009info:eu-repo/semantics/openAccessDegasperi,Giovanna R.Castilho,Roger F.Vercesi,Anibal E.eng2008-03-10T00:00:00Zoai:scielo:S0001-37652008000100009Revistahttp://www.scielo.br/aabchttps://old.scielo.br/oai/scielo-oai.php||aabc@abc.org.br1678-26900001-3765opendoar:2008-03-10T00:00Anais da Academia Brasileira de Ciências (Online) - Academia Brasileira de Ciências (ABC)false |
dc.title.none.fl_str_mv |
High susceptibility of activated lymphocytes to oxidative stress-induced cell death |
title |
High susceptibility of activated lymphocytes to oxidative stress-induced cell death |
spellingShingle |
High susceptibility of activated lymphocytes to oxidative stress-induced cell death Degasperi,Giovanna R. cell death free radicals immune response lymphopenia mitochondrial permeability transition spleen lymphocyte |
title_short |
High susceptibility of activated lymphocytes to oxidative stress-induced cell death |
title_full |
High susceptibility of activated lymphocytes to oxidative stress-induced cell death |
title_fullStr |
High susceptibility of activated lymphocytes to oxidative stress-induced cell death |
title_full_unstemmed |
High susceptibility of activated lymphocytes to oxidative stress-induced cell death |
title_sort |
High susceptibility of activated lymphocytes to oxidative stress-induced cell death |
author |
Degasperi,Giovanna R. |
author_facet |
Degasperi,Giovanna R. Castilho,Roger F. Vercesi,Anibal E. |
author_role |
author |
author2 |
Castilho,Roger F. Vercesi,Anibal E. |
author2_role |
author author |
dc.contributor.author.fl_str_mv |
Degasperi,Giovanna R. Castilho,Roger F. Vercesi,Anibal E. |
dc.subject.por.fl_str_mv |
cell death free radicals immune response lymphopenia mitochondrial permeability transition spleen lymphocyte |
topic |
cell death free radicals immune response lymphopenia mitochondrial permeability transition spleen lymphocyte |
description |
The present study provides evidence that activated spleen lymphocytes from Walker 256 tumor bearing rats are more susceptible than controls to tert-butyl hydroperoxide (t-BOOH)-induced necrotic cell death in vitro. The iron chelator and antioxidant deferoxamine, the intracellular Ca2+ chelator BAPTA, the L-type Ca2+ channel antagonist nifedipine or the mitochondrial permeability transition inhibitor cyclosporin A, but not the calcineurin inhibitor FK-506, render control and activated lymphocytes equally resistant to the toxic effects of t-BOOH. Incubation of activated lymphocytes in the presence of t-BOOH resulted in a cyclosporin A-sensitive decrease in mitochondrial membrane potential. These results indicate that the higher cytosolic Ca2+ level in activated lymphocytes increases their susceptibility to oxidative stress-induced cell death in a mechanism involving the participation of mitochondrial permeability transition. |
publishDate |
2008 |
dc.date.none.fl_str_mv |
2008-03-01 |
dc.type.driver.fl_str_mv |
info:eu-repo/semantics/article |
dc.type.status.fl_str_mv |
info:eu-repo/semantics/publishedVersion |
format |
article |
status_str |
publishedVersion |
dc.identifier.uri.fl_str_mv |
http://old.scielo.br/scielo.php?script=sci_arttext&pid=S0001-37652008000100009 |
url |
http://old.scielo.br/scielo.php?script=sci_arttext&pid=S0001-37652008000100009 |
dc.language.iso.fl_str_mv |
eng |
language |
eng |
dc.relation.none.fl_str_mv |
10.1590/S0001-37652008000100009 |
dc.rights.driver.fl_str_mv |
info:eu-repo/semantics/openAccess |
eu_rights_str_mv |
openAccess |
dc.format.none.fl_str_mv |
text/html |
dc.publisher.none.fl_str_mv |
Academia Brasileira de Ciências |
publisher.none.fl_str_mv |
Academia Brasileira de Ciências |
dc.source.none.fl_str_mv |
Anais da Academia Brasileira de Ciências v.80 n.1 2008 reponame:Anais da Academia Brasileira de Ciências (Online) instname:Academia Brasileira de Ciências (ABC) instacron:ABC |
instname_str |
Academia Brasileira de Ciências (ABC) |
instacron_str |
ABC |
institution |
ABC |
reponame_str |
Anais da Academia Brasileira de Ciências (Online) |
collection |
Anais da Academia Brasileira de Ciências (Online) |
repository.name.fl_str_mv |
Anais da Academia Brasileira de Ciências (Online) - Academia Brasileira de Ciências (ABC) |
repository.mail.fl_str_mv |
||aabc@abc.org.br |
_version_ |
1754302856904572928 |