Antioxidant dietary deficiency induces caspase activation in chick skeletal muscle cells
Autor(a) principal: | |
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Data de Publicação: | 2003 |
Outros Autores: | , , , , , |
Tipo de documento: | Artigo |
Idioma: | eng |
Título da fonte: | Brazilian Journal of Medical and Biological Research |
Texto Completo: | http://old.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2003000800010 |
Resumo: | Apoptosis and necrosis are two distinct forms of cell death that can occur in response to different agents and stress conditions. In order to verify if the oxidative stress induced by dietary selenium and vitamin E deficiencies can lead muscle cells to apoptosis, one-day-old chicks were reared using diets differing in their vitamin E (0 or 10 IU/kg) and selenium (0 or 0.15 ppm) supplementation. Chick skeletal muscle tissue was obtained from 28-day-old animals and used to verify apoptosis occurrence based on caspase activity detection and DNA fragmentation. Antioxidant deficiency significantly increased caspase-like activity assessed by the hydrolysis of fluorogenic peptide substrates (Abz-peptidyl-EDDnp) at lambdaexc = 320 nm and lambdaem = 420 nm. Proteolytic activation was not accompanied by typical internucleosomal DNA fragmentation detected by field inversion gel electrophoresis. Although the general caspase inhibitor N-benzyloxycarbonyl-Val-Ala-Asp(O-Me) fluoromethyl ketone (Z-VAD-fmk) (0 to 80 muM) did not block caspase-like activity when preincubated for 30 min with muscle homogenates, the hydrolyzed substrates presented the same cleavage profile in HPLC (at the aspartic acid residue) when incubated with the purified recombinant enzyme caspase-3. These data indicate that oxidative stress causes caspase-like activation in muscle cells and suggest that cell death associated with exudative diathesis (dietary deficiency of selenium and vitamin E) can follow the apoptotic pathway. |
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Brazilian Journal of Medical and Biological Research |
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Antioxidant dietary deficiency induces caspase activation in chick skeletal muscle cellsOxidative stressCaspase activationApoptosisDietary selenium deficiencyDietary vitamin E deficiencyInternucleosomal DNA fragmentationCaspase substrateApoptosis and necrosis are two distinct forms of cell death that can occur in response to different agents and stress conditions. In order to verify if the oxidative stress induced by dietary selenium and vitamin E deficiencies can lead muscle cells to apoptosis, one-day-old chicks were reared using diets differing in their vitamin E (0 or 10 IU/kg) and selenium (0 or 0.15 ppm) supplementation. Chick skeletal muscle tissue was obtained from 28-day-old animals and used to verify apoptosis occurrence based on caspase activity detection and DNA fragmentation. Antioxidant deficiency significantly increased caspase-like activity assessed by the hydrolysis of fluorogenic peptide substrates (Abz-peptidyl-EDDnp) at lambdaexc = 320 nm and lambdaem = 420 nm. Proteolytic activation was not accompanied by typical internucleosomal DNA fragmentation detected by field inversion gel electrophoresis. Although the general caspase inhibitor N-benzyloxycarbonyl-Val-Ala-Asp(O-Me) fluoromethyl ketone (Z-VAD-fmk) (0 to 80 muM) did not block caspase-like activity when preincubated for 30 min with muscle homogenates, the hydrolyzed substrates presented the same cleavage profile in HPLC (at the aspartic acid residue) when incubated with the purified recombinant enzyme caspase-3. These data indicate that oxidative stress causes caspase-like activation in muscle cells and suggest that cell death associated with exudative diathesis (dietary deficiency of selenium and vitamin E) can follow the apoptotic pathway.Associação Brasileira de Divulgação Científica2003-08-01info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersiontext/htmlhttp://old.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2003000800010Brazilian Journal of Medical and Biological Research v.36 n.8 2003reponame:Brazilian Journal of Medical and Biological Researchinstname:Associação Brasileira de Divulgação Científica (ABDC)instacron:ABDC10.1590/S0100-879X2003000800010info:eu-repo/semantics/openAccessNunes,V.A.Gozzo,A.J.Juliano,M.A.Cerqueira César,M.Sampaio,M.U.Sampaio,C.A.M.Araújo,M.S.eng2003-07-23T00:00:00Zoai:scielo:S0100-879X2003000800010Revistahttps://www.bjournal.org/https://old.scielo.br/oai/scielo-oai.phpbjournal@terra.com.br||bjournal@terra.com.br1414-431X0100-879Xopendoar:2003-07-23T00:00Brazilian Journal of Medical and Biological Research - Associação Brasileira de Divulgação Científica (ABDC)false |
dc.title.none.fl_str_mv |
Antioxidant dietary deficiency induces caspase activation in chick skeletal muscle cells |
title |
Antioxidant dietary deficiency induces caspase activation in chick skeletal muscle cells |
spellingShingle |
Antioxidant dietary deficiency induces caspase activation in chick skeletal muscle cells Nunes,V.A. Oxidative stress Caspase activation Apoptosis Dietary selenium deficiency Dietary vitamin E deficiency Internucleosomal DNA fragmentation Caspase substrate |
title_short |
Antioxidant dietary deficiency induces caspase activation in chick skeletal muscle cells |
title_full |
Antioxidant dietary deficiency induces caspase activation in chick skeletal muscle cells |
title_fullStr |
Antioxidant dietary deficiency induces caspase activation in chick skeletal muscle cells |
title_full_unstemmed |
Antioxidant dietary deficiency induces caspase activation in chick skeletal muscle cells |
title_sort |
Antioxidant dietary deficiency induces caspase activation in chick skeletal muscle cells |
author |
Nunes,V.A. |
author_facet |
Nunes,V.A. Gozzo,A.J. Juliano,M.A. Cerqueira César,M. Sampaio,M.U. Sampaio,C.A.M. Araújo,M.S. |
author_role |
author |
author2 |
Gozzo,A.J. Juliano,M.A. Cerqueira César,M. Sampaio,M.U. Sampaio,C.A.M. Araújo,M.S. |
author2_role |
author author author author author author |
dc.contributor.author.fl_str_mv |
Nunes,V.A. Gozzo,A.J. Juliano,M.A. Cerqueira César,M. Sampaio,M.U. Sampaio,C.A.M. Araújo,M.S. |
dc.subject.por.fl_str_mv |
Oxidative stress Caspase activation Apoptosis Dietary selenium deficiency Dietary vitamin E deficiency Internucleosomal DNA fragmentation Caspase substrate |
topic |
Oxidative stress Caspase activation Apoptosis Dietary selenium deficiency Dietary vitamin E deficiency Internucleosomal DNA fragmentation Caspase substrate |
description |
Apoptosis and necrosis are two distinct forms of cell death that can occur in response to different agents and stress conditions. In order to verify if the oxidative stress induced by dietary selenium and vitamin E deficiencies can lead muscle cells to apoptosis, one-day-old chicks were reared using diets differing in their vitamin E (0 or 10 IU/kg) and selenium (0 or 0.15 ppm) supplementation. Chick skeletal muscle tissue was obtained from 28-day-old animals and used to verify apoptosis occurrence based on caspase activity detection and DNA fragmentation. Antioxidant deficiency significantly increased caspase-like activity assessed by the hydrolysis of fluorogenic peptide substrates (Abz-peptidyl-EDDnp) at lambdaexc = 320 nm and lambdaem = 420 nm. Proteolytic activation was not accompanied by typical internucleosomal DNA fragmentation detected by field inversion gel electrophoresis. Although the general caspase inhibitor N-benzyloxycarbonyl-Val-Ala-Asp(O-Me) fluoromethyl ketone (Z-VAD-fmk) (0 to 80 muM) did not block caspase-like activity when preincubated for 30 min with muscle homogenates, the hydrolyzed substrates presented the same cleavage profile in HPLC (at the aspartic acid residue) when incubated with the purified recombinant enzyme caspase-3. These data indicate that oxidative stress causes caspase-like activation in muscle cells and suggest that cell death associated with exudative diathesis (dietary deficiency of selenium and vitamin E) can follow the apoptotic pathway. |
publishDate |
2003 |
dc.date.none.fl_str_mv |
2003-08-01 |
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=S0100-879X2003000800010 |
url |
http://old.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2003000800010 |
dc.language.iso.fl_str_mv |
eng |
language |
eng |
dc.relation.none.fl_str_mv |
10.1590/S0100-879X2003000800010 |
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 |
Associação Brasileira de Divulgação Científica |
publisher.none.fl_str_mv |
Associação Brasileira de Divulgação Científica |
dc.source.none.fl_str_mv |
Brazilian Journal of Medical and Biological Research v.36 n.8 2003 reponame:Brazilian Journal of Medical and Biological Research instname:Associação Brasileira de Divulgação Científica (ABDC) instacron:ABDC |
instname_str |
Associação Brasileira de Divulgação Científica (ABDC) |
instacron_str |
ABDC |
institution |
ABDC |
reponame_str |
Brazilian Journal of Medical and Biological Research |
collection |
Brazilian Journal of Medical and Biological Research |
repository.name.fl_str_mv |
Brazilian Journal of Medical and Biological Research - Associação Brasileira de Divulgação Científica (ABDC) |
repository.mail.fl_str_mv |
bjournal@terra.com.br||bjournal@terra.com.br |
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1754302932472299520 |