Efeito neuroprotetor do disseleneto de difenila sobre a memória, atividade locomotora e captação de cálcio frente a trauma mecano-encefálico em ratos
Autor(a) principal: | |
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Data de Publicação: | 2008 |
Tipo de documento: | Tese |
Idioma: | por |
Título da fonte: | Manancial - Repositório Digital da UFSM |
Texto Completo: | http://repositorio.ufsm.br/handle/1/28373 |
Resumo: | Cerebral concussion and traumatic brain injury (TBI) are a disturbance of neural function frequently induced by a sudden acceleration and deceleration forces of the head with or without skull fracture. A large number of studies have shown that the TBI is associated with various primary events like glutamate release, elevated intracellular calcium, the formation of free radicals and subsequent lipid peroxidation as well as the decrease of serum magnesium contents, behavior disturbances, like memory loss and damage on locomotor activities. Such primary events may cause secondary damage by activating endogenous autodestructive biochemical processes. Diphenyl diselenide (PhSe)2 is an organic selenium compound that has been demonstrated several biological effects that could be implicated in potential therapy to TBI. The aim of the present study was to evaluate the effects of the oral administration of (PhSe)2 on TBI rat model, using 45Ca+2 uptake in cortex, striatum and hippocampus slices and serum magnesium concentration. Moreover, there were evaluate some behavioral aspects using startle test, conditioned fear and spontaneous alternation tasks to evaluate the acquisition and facilitation of memory; open field and rota-rod task to evaluate the neurolocomotor activity. The present study there was possible to verify at dose administered an increase in 45Ca+2 uptake by cerebral cortex, striatum and hippocampus slices in animals subjected to TBI and which received (PhSe)2 treatment (100 mM 15 minutes post TBI event), especially at the pretreatment group (20 mM by 3 days and 100 mM 15 minutes post TBI event) when compared to TBI group. (PhSe)2 was effective to increase the serum magnesium levels concentration, which corroborate with its neuroprotective effect, once calcium and magnesium are present in several neurochemicals mechanism on Central Nervous System. Additionally, (PhSe)2 was able to ameliorate the acquisition and facilitation of memory in behavioral tasks performed,. Especially, when the (PhSe)2 was administered before and after to TBI. The neurolocomotor abilities were recorded at pre-training period (24h before to TBI). The behavioral changes in the open-field and rota-rod tasks were performed in 24 hours after TBI. (PhSe)2 was able to increase the locomotor activity in open-field task suggesting anxiolytic-like effect too. When (PhSe)2 was administered before and after to TBI. Finally, on rota-rod task reiterated the findings observed on open field, with a locomotor coordination response present in both (PhSe)2 treatments, once more with distinction to pretreatment. Therefore, considering the relevance of this study on the development of new drugs that can decrease the neuronal damage and improve the patients recover post TBI, decreasing sequels, our results suggest that the studies with (PhSe)2 against TBI could be more deeply investigated as a prospective pharmacological tools against TBI. |
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2023-03-24T13:58:37Z2023-03-24T13:58:37Z2008-12-22http://repositorio.ufsm.br/handle/1/28373Cerebral concussion and traumatic brain injury (TBI) are a disturbance of neural function frequently induced by a sudden acceleration and deceleration forces of the head with or without skull fracture. A large number of studies have shown that the TBI is associated with various primary events like glutamate release, elevated intracellular calcium, the formation of free radicals and subsequent lipid peroxidation as well as the decrease of serum magnesium contents, behavior disturbances, like memory loss and damage on locomotor activities. Such primary events may cause secondary damage by activating endogenous autodestructive biochemical processes. Diphenyl diselenide (PhSe)2 is an organic selenium compound that has been demonstrated several biological effects that could be implicated in potential therapy to TBI. The aim of the present study was to evaluate the effects of the oral administration of (PhSe)2 on TBI rat model, using 45Ca+2 uptake in cortex, striatum and hippocampus slices and serum magnesium concentration. Moreover, there were evaluate some behavioral aspects using startle test, conditioned fear and spontaneous alternation tasks to evaluate the acquisition and facilitation of memory; open field and rota-rod task to evaluate the neurolocomotor activity. The present study there was possible to verify at dose administered an increase in 45Ca+2 uptake by cerebral cortex, striatum and hippocampus slices in animals subjected to TBI and which received (PhSe)2 treatment (100 mM 15 minutes post TBI event), especially at the pretreatment group (20 mM by 3 days and 100 mM 15 minutes post TBI event) when compared to TBI group. (PhSe)2 was effective to increase the serum magnesium levels concentration, which corroborate with its neuroprotective effect, once calcium and magnesium are present in several neurochemicals mechanism on Central Nervous System. Additionally, (PhSe)2 was able to ameliorate the acquisition and facilitation of memory in behavioral tasks performed,. Especially, when the (PhSe)2 was administered before and after to TBI. The neurolocomotor abilities were recorded at pre-training period (24h before to TBI). The behavioral changes in the open-field and rota-rod tasks were performed in 24 hours after TBI. (PhSe)2 was able to increase the locomotor activity in open-field task suggesting anxiolytic-like effect too. When (PhSe)2 was administered before and after to TBI. Finally, on rota-rod task reiterated the findings observed on open field, with a locomotor coordination response present in both (PhSe)2 treatments, once more with distinction to pretreatment. Therefore, considering the relevance of this study on the development of new drugs that can decrease the neuronal damage and improve the patients recover post TBI, decreasing sequels, our results suggest that the studies with (PhSe)2 against TBI could be more deeply investigated as a prospective pharmacological tools against TBI.As concussões e traumas encefálicos (TBI) são distúrbios imputados às funções cerebrais freqüentemente provocados por forças de aceleração e desaceleração na caixa craniana com ou sem fraturas. Um extenso número de estudos tem demonstrado que o TBI está associado a vários eventos primários, tais como liberação de glutamato, elevação intracelular das concentrações de cálcio, geração de radicais livres, diminuição da concentração sérica de magnésio, alterações comportamentais relacionadas com a perda de memória e prejuízo na atividade locomotora, dentre outras. Tais eventos podem causar danos secundários pela ativação de processos bioquímicos endógenos autodestrutivos. O disseleneto de difenila (PhSe)2 é um composto orgânico à base de selênio que tem demonstrado vários efeitos biológicos, os quais podem ser adicional e potencialmente efetivos à terapia do TBI. A cooperação deste estudo mostra-se interessante pela avaliação da administração oral de (PhSe)2 frente a um modelo de trauma induzido em ratos usando como parâmetros avaliativos a recaptação de 45Ca+2 membranar em fatias de córtex, estriado e hipocampo; a dosagem sérica dos níveis de magnésio; a aquisição e facilitação de memória através dos testes do medo condicionado, alternação espontânea e estímulo auditório; a atividade locomotora através dos testes de campo aberto e rota-rod. Neste estudo foi possível verificar o aumento da captação de 45Ca+2 membranar nas fatias de córtex, estriado e hipocampo em todos os animais que foram submetidos ao trauma e ao tratamento oral de (PhSe)2 (100 mM, 15 minutos após o TBI), especialmente aos que receberam pré-tratamento e tratamento (20 mM por 3 dias que antecederam o trauma e 100 mM, 15 minutos após o TBI), quando comparados aos animais que foram submetidos somente ao TBI. O (PhSe)2 foi efetivo em aumentar os níveis séricos de magnésio, o que corrobora com seu efeito neuroprotetor, uma vez que os íons cálcio e magnésio estão presentes em vários mecanismos neuroquímicos do Sistema Nervoso Central (SNC). Somado a estas ações, o (PhSe)2 foi capaz de melhorar a aquisição e facilitação de memória, demonstrando neuroproteção sobre os parâmetros comportamentais utilizados. De forma especial, quando o (PhSe)2 foi administrado antes e depois da indução do TBI. As habilidades locomotoras foram registradas em sessõestreinos e as alterações comportamentais pós-trauma foram realizadas 24 horas após indução do TBI e tratamentos. O (PhSe)2 melhorou a atividade locomotora observada no teste de campo aberto, demonstrando, ainda, um efeito ansiolítico, de modo especial quando o (PhSe)2 foi administrado antes e depois do TBI. Finalmente, o teste rota-rod reiterou os achados relacionados à locomoção observados no teste de campo aberto, com uma resposta de coordenação motora presente em ambos os tratamentos com (PhSe)2, porém, com distinção ao grupo que recebeu pré-tratamento e tratamento pós trauma. Diante disto, considerando a relevância deste estudo para o desenvolvimento de novos fármacos que possam diminuir o dano das células neurais e melhorar a recuperação de pacientes pós-trauma, diminuindo seqüelas, nossos resultados sugerem que os estudos sobre (PhSe)2 frente ao TBI possam ser aprofundados e melhor investigados para seu possível emprego como ferramenta farmacológica contra o TBI.porUniversidade Federal de Santa MariaCentro de Ciências Naturais e ExatasPrograma de Pós-Graduação em Ciências Biológicas: Bioquímica ToxicológicaUFSMBrasilBioquímicaAttribution-NonCommercial-NoDerivatives 4.0 Internationalhttp://creativecommons.org/licenses/by-nc-nd/4.0/info:eu-repo/semantics/openAccessSelênioTrauma encefálicoCálcioMagnésioMemóriaAtividade locomotoraSeleniumTrauma brain injuryCalciumMagnesiumMemoryLocomotor activityCNPQ::CIENCIAS BIOLOGICAS::BIOQUIMICAEfeito neuroprotetor do disseleneto de difenila sobre a memória, atividade locomotora e captação de cálcio frente a trauma mecano-encefálico em ratosNeuroprotective effect of diphenyl diselenide on membrane viability, memory and locomotor activity after mechanic trauma brain injury (TBI) induction in ratsinfo:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/doctoralThesisNogueira, Cristina Waynehttp://lattes.cnpq.br/2877042401245169Rocha, João Batista Teixeira daSoares, Félix Alexandre AntunesSchetinger, Maria Rosa ChitolinaBürguer, Marilise EscobarBarbosa, Nilda Berenice de Vargashttp://lattes.cnpq.br/4839195121781005Oliveira, Luís Flávio Souza de2008000000026006006006000186436d-f662-4a5e-b36e-8c8ab8e10bf8263759d6-1d0b-4312-87d3-d1ebaeaa23e24a2aa8a7-cae4-4911-ab61-026ad02d652097b2e117-480f-4e1c-a62b-9dab79cb9fd393acb9e6-39fa-412c-84a4-a90a4863b53ef506246d-4af2-46cc-a9ff-66601e96abcd358cdf1a-0ca8-44bd-8d8d-bb5bec532515reponame:Manancial - Repositório Digital da UFSMinstname:Universidade Federal de Santa Maria (UFSM)instacron:UFSMORIGINALTES_PPGBT_2008_OLIVEIRA_LUIS.pdfTES_PPGBT_2008_OLIVEIRA_LUIS.pdfTese de Doutoradoapplication/pdf784640http://repositorio.ufsm.br/bitstream/1/28373/1/TES_PPGBT_2008_OLIVEIRA_LUIS.pdfda9d5767b0c9bad89b0739aa6175d4e6MD51CC-LICENSElicense_rdflicense_rdfapplication/rdf+xml; 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dc.title.por.fl_str_mv |
Efeito neuroprotetor do disseleneto de difenila sobre a memória, atividade locomotora e captação de cálcio frente a trauma mecano-encefálico em ratos |
dc.title.alternative.eng.fl_str_mv |
Neuroprotective effect of diphenyl diselenide on membrane viability, memory and locomotor activity after mechanic trauma brain injury (TBI) induction in rats |
title |
Efeito neuroprotetor do disseleneto de difenila sobre a memória, atividade locomotora e captação de cálcio frente a trauma mecano-encefálico em ratos |
spellingShingle |
Efeito neuroprotetor do disseleneto de difenila sobre a memória, atividade locomotora e captação de cálcio frente a trauma mecano-encefálico em ratos Oliveira, Luís Flávio Souza de Selênio Trauma encefálico Cálcio Magnésio Memória Atividade locomotora Selenium Trauma brain injury Calcium Magnesium Memory Locomotor activity CNPQ::CIENCIAS BIOLOGICAS::BIOQUIMICA |
title_short |
Efeito neuroprotetor do disseleneto de difenila sobre a memória, atividade locomotora e captação de cálcio frente a trauma mecano-encefálico em ratos |
title_full |
Efeito neuroprotetor do disseleneto de difenila sobre a memória, atividade locomotora e captação de cálcio frente a trauma mecano-encefálico em ratos |
title_fullStr |
Efeito neuroprotetor do disseleneto de difenila sobre a memória, atividade locomotora e captação de cálcio frente a trauma mecano-encefálico em ratos |
title_full_unstemmed |
Efeito neuroprotetor do disseleneto de difenila sobre a memória, atividade locomotora e captação de cálcio frente a trauma mecano-encefálico em ratos |
title_sort |
Efeito neuroprotetor do disseleneto de difenila sobre a memória, atividade locomotora e captação de cálcio frente a trauma mecano-encefálico em ratos |
author |
Oliveira, Luís Flávio Souza de |
author_facet |
Oliveira, Luís Flávio Souza de |
author_role |
author |
dc.contributor.advisor1.fl_str_mv |
Nogueira, Cristina Wayne |
dc.contributor.advisor1Lattes.fl_str_mv |
http://lattes.cnpq.br/2877042401245169 |
dc.contributor.advisor-co1.fl_str_mv |
Rocha, João Batista Teixeira da |
dc.contributor.referee1.fl_str_mv |
Soares, Félix Alexandre Antunes |
dc.contributor.referee2.fl_str_mv |
Schetinger, Maria Rosa Chitolina |
dc.contributor.referee3.fl_str_mv |
Bürguer, Marilise Escobar |
dc.contributor.referee4.fl_str_mv |
Barbosa, Nilda Berenice de Vargas |
dc.contributor.authorLattes.fl_str_mv |
http://lattes.cnpq.br/4839195121781005 |
dc.contributor.author.fl_str_mv |
Oliveira, Luís Flávio Souza de |
contributor_str_mv |
Nogueira, Cristina Wayne Rocha, João Batista Teixeira da Soares, Félix Alexandre Antunes Schetinger, Maria Rosa Chitolina Bürguer, Marilise Escobar Barbosa, Nilda Berenice de Vargas |
dc.subject.por.fl_str_mv |
Selênio Trauma encefálico Cálcio Magnésio Memória Atividade locomotora |
topic |
Selênio Trauma encefálico Cálcio Magnésio Memória Atividade locomotora Selenium Trauma brain injury Calcium Magnesium Memory Locomotor activity CNPQ::CIENCIAS BIOLOGICAS::BIOQUIMICA |
dc.subject.eng.fl_str_mv |
Selenium Trauma brain injury Calcium Magnesium Memory Locomotor activity |
dc.subject.cnpq.fl_str_mv |
CNPQ::CIENCIAS BIOLOGICAS::BIOQUIMICA |
description |
Cerebral concussion and traumatic brain injury (TBI) are a disturbance of neural function frequently induced by a sudden acceleration and deceleration forces of the head with or without skull fracture. A large number of studies have shown that the TBI is associated with various primary events like glutamate release, elevated intracellular calcium, the formation of free radicals and subsequent lipid peroxidation as well as the decrease of serum magnesium contents, behavior disturbances, like memory loss and damage on locomotor activities. Such primary events may cause secondary damage by activating endogenous autodestructive biochemical processes. Diphenyl diselenide (PhSe)2 is an organic selenium compound that has been demonstrated several biological effects that could be implicated in potential therapy to TBI. The aim of the present study was to evaluate the effects of the oral administration of (PhSe)2 on TBI rat model, using 45Ca+2 uptake in cortex, striatum and hippocampus slices and serum magnesium concentration. Moreover, there were evaluate some behavioral aspects using startle test, conditioned fear and spontaneous alternation tasks to evaluate the acquisition and facilitation of memory; open field and rota-rod task to evaluate the neurolocomotor activity. The present study there was possible to verify at dose administered an increase in 45Ca+2 uptake by cerebral cortex, striatum and hippocampus slices in animals subjected to TBI and which received (PhSe)2 treatment (100 mM 15 minutes post TBI event), especially at the pretreatment group (20 mM by 3 days and 100 mM 15 minutes post TBI event) when compared to TBI group. (PhSe)2 was effective to increase the serum magnesium levels concentration, which corroborate with its neuroprotective effect, once calcium and magnesium are present in several neurochemicals mechanism on Central Nervous System. Additionally, (PhSe)2 was able to ameliorate the acquisition and facilitation of memory in behavioral tasks performed,. Especially, when the (PhSe)2 was administered before and after to TBI. The neurolocomotor abilities were recorded at pre-training period (24h before to TBI). The behavioral changes in the open-field and rota-rod tasks were performed in 24 hours after TBI. (PhSe)2 was able to increase the locomotor activity in open-field task suggesting anxiolytic-like effect too. When (PhSe)2 was administered before and after to TBI. Finally, on rota-rod task reiterated the findings observed on open field, with a locomotor coordination response present in both (PhSe)2 treatments, once more with distinction to pretreatment. Therefore, considering the relevance of this study on the development of new drugs that can decrease the neuronal damage and improve the patients recover post TBI, decreasing sequels, our results suggest that the studies with (PhSe)2 against TBI could be more deeply investigated as a prospective pharmacological tools against TBI. |
publishDate |
2008 |
dc.date.issued.fl_str_mv |
2008-12-22 |
dc.date.accessioned.fl_str_mv |
2023-03-24T13:58:37Z |
dc.date.available.fl_str_mv |
2023-03-24T13:58:37Z |
dc.type.status.fl_str_mv |
info:eu-repo/semantics/publishedVersion |
dc.type.driver.fl_str_mv |
info:eu-repo/semantics/doctoralThesis |
format |
doctoralThesis |
status_str |
publishedVersion |
dc.identifier.uri.fl_str_mv |
http://repositorio.ufsm.br/handle/1/28373 |
url |
http://repositorio.ufsm.br/handle/1/28373 |
dc.language.iso.fl_str_mv |
por |
language |
por |
dc.relation.cnpq.fl_str_mv |
200800000002 |
dc.relation.confidence.fl_str_mv |
600 600 600 600 |
dc.relation.authority.fl_str_mv |
0186436d-f662-4a5e-b36e-8c8ab8e10bf8 263759d6-1d0b-4312-87d3-d1ebaeaa23e2 4a2aa8a7-cae4-4911-ab61-026ad02d6520 97b2e117-480f-4e1c-a62b-9dab79cb9fd3 93acb9e6-39fa-412c-84a4-a90a4863b53e f506246d-4af2-46cc-a9ff-66601e96abcd 358cdf1a-0ca8-44bd-8d8d-bb5bec532515 |
dc.rights.driver.fl_str_mv |
Attribution-NonCommercial-NoDerivatives 4.0 International http://creativecommons.org/licenses/by-nc-nd/4.0/ info:eu-repo/semantics/openAccess |
rights_invalid_str_mv |
Attribution-NonCommercial-NoDerivatives 4.0 International http://creativecommons.org/licenses/by-nc-nd/4.0/ |
eu_rights_str_mv |
openAccess |
dc.publisher.none.fl_str_mv |
Universidade Federal de Santa Maria Centro de Ciências Naturais e Exatas |
dc.publisher.program.fl_str_mv |
Programa de Pós-Graduação em Ciências Biológicas: Bioquímica Toxicológica |
dc.publisher.initials.fl_str_mv |
UFSM |
dc.publisher.country.fl_str_mv |
Brasil |
dc.publisher.department.fl_str_mv |
Bioquímica |
publisher.none.fl_str_mv |
Universidade Federal de Santa Maria Centro de Ciências Naturais e Exatas |
dc.source.none.fl_str_mv |
reponame:Manancial - Repositório Digital da UFSM instname:Universidade Federal de Santa Maria (UFSM) instacron:UFSM |
instname_str |
Universidade Federal de Santa Maria (UFSM) |
instacron_str |
UFSM |
institution |
UFSM |
reponame_str |
Manancial - Repositório Digital da UFSM |
collection |
Manancial - Repositório Digital da UFSM |
bitstream.url.fl_str_mv |
http://repositorio.ufsm.br/bitstream/1/28373/1/TES_PPGBT_2008_OLIVEIRA_LUIS.pdf http://repositorio.ufsm.br/bitstream/1/28373/2/license_rdf http://repositorio.ufsm.br/bitstream/1/28373/3/license.txt |
bitstream.checksum.fl_str_mv |
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MD5 MD5 MD5 |
repository.name.fl_str_mv |
Manancial - Repositório Digital da UFSM - Universidade Federal de Santa Maria (UFSM) |
repository.mail.fl_str_mv |
|
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1801223706481000448 |