Ischemic preconditioning reduces peripheral oxidative damage associated with brain ischemia in rats
Autor(a) principal: | |
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Data de Publicação: | 1999 |
Outros Autores: | , , , |
Tipo de documento: | Artigo |
Idioma: | eng |
Título da fonte: | Repositório Institucional da UFRGS |
Texto Completo: | http://hdl.handle.net/10183/21163 |
Resumo: | Brain ischemia followed by reperfusion causes neuronal death related to oxidative damage. Furthermore, it has been reported that subjects suffering from ischemic cerebrovascular disorders exhibit changes in circulating platelet aggregation, a characteristic that might be important for their clinical outcome. In the present investigation we studied tert-butyl hydroperoxide-initiated plasma chemiluminescence and thiol content as measures of peripheral oxidative damage in naive and preconditioned rats submitted to forebrain ischemia produced by the 4-vessel occlusion method. Rats were submitted to 2 or 10 min of global transient forebrain ischemia followed by 60 min or 1, 2, 5, 10 or 30 days of reperfusion. Preconditioned rats were submitted to a 10- min ischemic episode 1 day after a 2-min ischemic event (2 + 10 min), followed by 60 min or 1 or 2 days of reperfusion. It has been demonstrated that such preconditioning protects against neuronal death in rats and gerbils submitted to a lethal (10 min) ischemic episode. The results show that both 2 and 10 min of ischemia cause an increase of plasma chemiluminescence when compared to control and sham rats. In the 2-min ischemic group, the effect was not present after reperfusion. In the 10-min ischemic group, the increase was present up to 1 day after recirculation and values returned to control levels after 2 days. However, rats preconditioned to ischemia (2 + 10 min) and reperfusion showed no differences in plasma chemiluminescence when compared to controls. We also analyzed plasma thiol content since it has been described that sulfhydryl (SH) groups significantly contribute to the antioxidant capacity of plasma. There was a significant decrease of plasma thiol content after 2, 10 and 2 + 10 min of ischemia followed by reperfusion when compared to controls. We conclude that ischemia may cause, along with brain oxidative damage and cell death, a peripheral oxidative damage that is reduced by the preconditioning phenomenon. |
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Frassetto, Silvana SorianoSchetinger, Maria Rosa ChitolinaWebber, AnalupeSarkis, João José FreitasNetto, Carlos Alexandre2010-04-24T04:15:33Z19990100-879Xhttp://hdl.handle.net/10183/21163000297357Brain ischemia followed by reperfusion causes neuronal death related to oxidative damage. Furthermore, it has been reported that subjects suffering from ischemic cerebrovascular disorders exhibit changes in circulating platelet aggregation, a characteristic that might be important for their clinical outcome. In the present investigation we studied tert-butyl hydroperoxide-initiated plasma chemiluminescence and thiol content as measures of peripheral oxidative damage in naive and preconditioned rats submitted to forebrain ischemia produced by the 4-vessel occlusion method. Rats were submitted to 2 or 10 min of global transient forebrain ischemia followed by 60 min or 1, 2, 5, 10 or 30 days of reperfusion. Preconditioned rats were submitted to a 10- min ischemic episode 1 day after a 2-min ischemic event (2 + 10 min), followed by 60 min or 1 or 2 days of reperfusion. It has been demonstrated that such preconditioning protects against neuronal death in rats and gerbils submitted to a lethal (10 min) ischemic episode. The results show that both 2 and 10 min of ischemia cause an increase of plasma chemiluminescence when compared to control and sham rats. In the 2-min ischemic group, the effect was not present after reperfusion. In the 10-min ischemic group, the increase was present up to 1 day after recirculation and values returned to control levels after 2 days. However, rats preconditioned to ischemia (2 + 10 min) and reperfusion showed no differences in plasma chemiluminescence when compared to controls. We also analyzed plasma thiol content since it has been described that sulfhydryl (SH) groups significantly contribute to the antioxidant capacity of plasma. There was a significant decrease of plasma thiol content after 2, 10 and 2 + 10 min of ischemia followed by reperfusion when compared to controls. We conclude that ischemia may cause, along with brain oxidative damage and cell death, a peripheral oxidative damage that is reduced by the preconditioning phenomenon.application/pdfengBrazilian journal of medical and biological research = Revista brasileira de pesquisas médicas e biológicas. Ribeirão Preto, SP. Vol. 32, no. 10 (Oct. 1999), p. 1295-1302BioquímicaBrain ischemiaIschemic preconditioningOxidative damageHydroperoxide-initiated chemiluminescencePlasma thiolsIschemic preconditioning reduces peripheral oxidative damage associated with brain ischemia in ratsinfo:eu-repo/semantics/articleinfo:eu-repo/semantics/otherinfo:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/openAccessreponame:Repositório Institucional da UFRGSinstname:Universidade Federal do Rio Grande do Sul (UFRGS)instacron:UFRGSORIGINAL000297357.pdf000297357.pdfTexto completo (inglês)application/pdf116574http://www.lume.ufrgs.br/bitstream/10183/21163/1/000297357.pdf4d75e328e229977179d3fd7f758abfa0MD51TEXT000297357.pdf.txt000297357.pdf.txtExtracted Texttext/plain29601http://www.lume.ufrgs.br/bitstream/10183/21163/2/000297357.pdf.txtb7e04c2dee8b54289ff82d1f6b46a4a6MD52THUMBNAIL000297357.pdf.jpg000297357.pdf.jpgGenerated Thumbnailimage/jpeg1667http://www.lume.ufrgs.br/bitstream/10183/21163/3/000297357.pdf.jpg0ed46006c898d41f935b33ee60cf05abMD5310183/211632021-11-20 06:01:11.583365oai:www.lume.ufrgs.br:10183/21163Repositório de PublicaçõesPUBhttps://lume.ufrgs.br/oai/requestopendoar:2021-11-20T08:01:11Repositório Institucional da UFRGS - Universidade Federal do Rio Grande do Sul (UFRGS)false |
dc.title.pt_BR.fl_str_mv |
Ischemic preconditioning reduces peripheral oxidative damage associated with brain ischemia in rats |
title |
Ischemic preconditioning reduces peripheral oxidative damage associated with brain ischemia in rats |
spellingShingle |
Ischemic preconditioning reduces peripheral oxidative damage associated with brain ischemia in rats Frassetto, Silvana Soriano Bioquímica Brain ischemia Ischemic preconditioning Oxidative damage Hydroperoxide-initiated chemiluminescence Plasma thiols |
title_short |
Ischemic preconditioning reduces peripheral oxidative damage associated with brain ischemia in rats |
title_full |
Ischemic preconditioning reduces peripheral oxidative damage associated with brain ischemia in rats |
title_fullStr |
Ischemic preconditioning reduces peripheral oxidative damage associated with brain ischemia in rats |
title_full_unstemmed |
Ischemic preconditioning reduces peripheral oxidative damage associated with brain ischemia in rats |
title_sort |
Ischemic preconditioning reduces peripheral oxidative damage associated with brain ischemia in rats |
author |
Frassetto, Silvana Soriano |
author_facet |
Frassetto, Silvana Soriano Schetinger, Maria Rosa Chitolina Webber, Analupe Sarkis, João José Freitas Netto, Carlos Alexandre |
author_role |
author |
author2 |
Schetinger, Maria Rosa Chitolina Webber, Analupe Sarkis, João José Freitas Netto, Carlos Alexandre |
author2_role |
author author author author |
dc.contributor.author.fl_str_mv |
Frassetto, Silvana Soriano Schetinger, Maria Rosa Chitolina Webber, Analupe Sarkis, João José Freitas Netto, Carlos Alexandre |
dc.subject.por.fl_str_mv |
Bioquímica |
topic |
Bioquímica Brain ischemia Ischemic preconditioning Oxidative damage Hydroperoxide-initiated chemiluminescence Plasma thiols |
dc.subject.eng.fl_str_mv |
Brain ischemia Ischemic preconditioning Oxidative damage Hydroperoxide-initiated chemiluminescence Plasma thiols |
description |
Brain ischemia followed by reperfusion causes neuronal death related to oxidative damage. Furthermore, it has been reported that subjects suffering from ischemic cerebrovascular disorders exhibit changes in circulating platelet aggregation, a characteristic that might be important for their clinical outcome. In the present investigation we studied tert-butyl hydroperoxide-initiated plasma chemiluminescence and thiol content as measures of peripheral oxidative damage in naive and preconditioned rats submitted to forebrain ischemia produced by the 4-vessel occlusion method. Rats were submitted to 2 or 10 min of global transient forebrain ischemia followed by 60 min or 1, 2, 5, 10 or 30 days of reperfusion. Preconditioned rats were submitted to a 10- min ischemic episode 1 day after a 2-min ischemic event (2 + 10 min), followed by 60 min or 1 or 2 days of reperfusion. It has been demonstrated that such preconditioning protects against neuronal death in rats and gerbils submitted to a lethal (10 min) ischemic episode. The results show that both 2 and 10 min of ischemia cause an increase of plasma chemiluminescence when compared to control and sham rats. In the 2-min ischemic group, the effect was not present after reperfusion. In the 10-min ischemic group, the increase was present up to 1 day after recirculation and values returned to control levels after 2 days. However, rats preconditioned to ischemia (2 + 10 min) and reperfusion showed no differences in plasma chemiluminescence when compared to controls. We also analyzed plasma thiol content since it has been described that sulfhydryl (SH) groups significantly contribute to the antioxidant capacity of plasma. There was a significant decrease of plasma thiol content after 2, 10 and 2 + 10 min of ischemia followed by reperfusion when compared to controls. We conclude that ischemia may cause, along with brain oxidative damage and cell death, a peripheral oxidative damage that is reduced by the preconditioning phenomenon. |
publishDate |
1999 |
dc.date.issued.fl_str_mv |
1999 |
dc.date.accessioned.fl_str_mv |
2010-04-24T04:15:33Z |
dc.type.driver.fl_str_mv |
info:eu-repo/semantics/article info:eu-repo/semantics/other |
dc.type.status.fl_str_mv |
info:eu-repo/semantics/publishedVersion |
format |
article |
status_str |
publishedVersion |
dc.identifier.uri.fl_str_mv |
http://hdl.handle.net/10183/21163 |
dc.identifier.issn.pt_BR.fl_str_mv |
0100-879X |
dc.identifier.nrb.pt_BR.fl_str_mv |
000297357 |
identifier_str_mv |
0100-879X 000297357 |
url |
http://hdl.handle.net/10183/21163 |
dc.language.iso.fl_str_mv |
eng |
language |
eng |
dc.relation.ispartof.pt_BR.fl_str_mv |
Brazilian journal of medical and biological research = Revista brasileira de pesquisas médicas e biológicas. Ribeirão Preto, SP. Vol. 32, no. 10 (Oct. 1999), p. 1295-1302 |
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openAccess |
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