Efeito protetor da N-acetilcisteína sobre o estresse oxidativo causado pela administração crônica de aspartame em ratos
Autor(a) principal: | |
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Data de Publicação: | 2015 |
Tipo de documento: | Tese |
Idioma: | por |
Título da fonte: | Repositório Institucional Manancial UFSM |
Texto Completo: | http://repositorio.ufsm.br/handle/1/17558 |
Resumo: | This thesis evaluated the N-acetylcysteine effects (150 mg/kg, intraperitoneal) on the biochemical and oxidative changes caused by the daily oral consumption of aspartame at 40 mg/kg for six weeks by rats. For this purpose, were performed two experiments, in both the animals were divided in four groups: Control – received both aspartame and Nacetylcysteine vehicles; NAC – received aspartame vehicle, and N-acetylcysteine; ASP – received aspartame, and N-acetylcysteine vehicle; ASP-NAC – received both aspartame and N-acetylcysteine. The aspartame was administrated for six weeks; whereas the Nacetylcysteine was injected only in the fifth and sixth week. After it, the animals were anesthetized, their blood was removed, the serum was separated; and then, the rats were euthanized by exsanguination. In the first experiment, the serum was used for the measurement of glucose levels and also biomarkers of kidney and liver damage; the whole brain, liver and kidney were removed for the analysis of the oxidative stress parameters. As the results, in general, aspartame caused hyperglycemia and oxidative stress in the whole brain, and hepatic and renal tissues. N-acetylcysteine treatment protected all these tissues against the oxidative damage (lipid peroxidation and protein carbonylation), in especial, by promoting the reduced glutathione (GSH) synthesis, inducing the enzymes related to its metabolism (glutathione peroxidase (GPx), glutathione reductase (GR) and glutathione Stransferase), and elevating the ascorbic acid levels and total reactive antioxidant potential. In the second experiment, the serum was utilized for the determination of glucose content and lipid profile; the liver was removed for glucose measurement; and the whole brain was separated in the following structures: cerebral cortex, cerebellum, brainstem, and hypothalamus; in which was held the research of the oxidative stress biomarkers. The aspartame consumption caused an elevated glucose production in the liver, hyperglycemia, hypertriglyceridemia, hypercholesterolemia; and oxidative stress in all the brain regions. Although N-acetylcysteine treatment did not reduce neither the synthesis of liver glucose nor the hyperglycemia, it normalized the triglycerides and high-density lipoprotein cholesterol in the serum. This antioxidative treatment also protected all the brain regions against the lipid peroxidation, increased GSH levels and induced its associated enzymes (GPx and GR), triggering different defensive responses according each brain region. Therefore, the data of this thesis suggest that N-acetylcysteine attenuates the oxidative damage generated by the intake of this artificial sweetener. More studies were needed to elucidate the signaling pathways involved in this process; as well as to determine the aspartame metabolites levels (phenylalanine, aspartate and methanol) found in the rat plasma and brain. |
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2019-07-25T17:35:24Z2019-07-25T17:35:24Z2015-03-12http://repositorio.ufsm.br/handle/1/17558This thesis evaluated the N-acetylcysteine effects (150 mg/kg, intraperitoneal) on the biochemical and oxidative changes caused by the daily oral consumption of aspartame at 40 mg/kg for six weeks by rats. For this purpose, were performed two experiments, in both the animals were divided in four groups: Control – received both aspartame and Nacetylcysteine vehicles; NAC – received aspartame vehicle, and N-acetylcysteine; ASP – received aspartame, and N-acetylcysteine vehicle; ASP-NAC – received both aspartame and N-acetylcysteine. The aspartame was administrated for six weeks; whereas the Nacetylcysteine was injected only in the fifth and sixth week. After it, the animals were anesthetized, their blood was removed, the serum was separated; and then, the rats were euthanized by exsanguination. In the first experiment, the serum was used for the measurement of glucose levels and also biomarkers of kidney and liver damage; the whole brain, liver and kidney were removed for the analysis of the oxidative stress parameters. As the results, in general, aspartame caused hyperglycemia and oxidative stress in the whole brain, and hepatic and renal tissues. N-acetylcysteine treatment protected all these tissues against the oxidative damage (lipid peroxidation and protein carbonylation), in especial, by promoting the reduced glutathione (GSH) synthesis, inducing the enzymes related to its metabolism (glutathione peroxidase (GPx), glutathione reductase (GR) and glutathione Stransferase), and elevating the ascorbic acid levels and total reactive antioxidant potential. In the second experiment, the serum was utilized for the determination of glucose content and lipid profile; the liver was removed for glucose measurement; and the whole brain was separated in the following structures: cerebral cortex, cerebellum, brainstem, and hypothalamus; in which was held the research of the oxidative stress biomarkers. The aspartame consumption caused an elevated glucose production in the liver, hyperglycemia, hypertriglyceridemia, hypercholesterolemia; and oxidative stress in all the brain regions. Although N-acetylcysteine treatment did not reduce neither the synthesis of liver glucose nor the hyperglycemia, it normalized the triglycerides and high-density lipoprotein cholesterol in the serum. This antioxidative treatment also protected all the brain regions against the lipid peroxidation, increased GSH levels and induced its associated enzymes (GPx and GR), triggering different defensive responses according each brain region. Therefore, the data of this thesis suggest that N-acetylcysteine attenuates the oxidative damage generated by the intake of this artificial sweetener. More studies were needed to elucidate the signaling pathways involved in this process; as well as to determine the aspartame metabolites levels (phenylalanine, aspartate and methanol) found in the rat plasma and brain.Esta tese avaliou os efeitos da N-acetilcisteína (150 mg/kg, intraperitoneal) frente às alterações bioquímicas e oxidativas ocasionadas pelo consumo oral diário de 40 mg/kg aspartame durante seis semanas por ratos. Para isto, foram realizados dois experimentos, onde, em ambos, os animais foram divididos em quatro grupos: Controle – receberam ambos os veículos, o do aspartame e o da N-acetilcisteína; NAC – receberam o veículo do aspartame, e a N-acetilcisteína; ASP – receberam o aspartame, e o veículo da Nacetilcisteína; ASP-NAC – receberam o aspartame e a N-acetilcisteína. O aspartame foi administrado durante seis semanas; enquanto que a N-acetilcisteína foi injetada apenas na quinta e sexta semana. Depois disto, os animais foram anestesiados, o sangue deles foi retirado, e o soro separado; e então, os ratos foram eutanasiados por exsanguinação. No primeiro experimento, o soro foi usado para a medida de glicose e dos biomarcadores de dano hepático e renal; o cérebro inteiro, o fígado e os rins foram removidos para análise dos parâmetros de estresse oxidativo. Conforme os resultados obtidos, de maneira geral, o aspartame ocasionou hiperglicemia e estresse oxidativo no cérebro inteiro e nos tecidos hepático e renal. O tratamento com N-acetilcisteína protegeu todos os tecidos estudados contra o dano oxidativo (peroxidação lipídica e carbonilação proteica), especialmente, por promover a síntese de glutationa reduzida (GSH), induzir as enzimas relacionadas ao metabolismo da mesma (glutationa peroxidase (GPx), glutationa redutase (GR) e glutationa S-transferase), e elevar os níveis de ácido ascórbico e o potencial reativo antioxidante total. No segundo experimento, o soro foi utilizado para a determinação de glicose e do perfil lipídico; o fígado foi retirado para a medida de glicose; e o cérebro inteiro foi separado nas seguintes estruturas: córtex cerebral, cerebelo, tronco encefálico, e hipotálamo; nas quais foi realizada a pesquisa de biomarcadores de estresse oxidativo. O consumo do aspartame causou uma produção elevada de glicose no fígado, hiperglicemia, hipertrigliceridemia e hipercolesterolemia; e, estresse oxidativo em todas as estruturas encefálicas. Embora o tratamento com a N-acetilcisteína não tenha reduzido a síntese de glicose hepática e nem a hiperglicemia, ela normalizou os níveis de triglicerídeos e de lipoproteína de alta densidade no soro. Este tratamento antioxidante também protegeu todas as estruturas encefálicas contra a peroxidação lipídica, aumentou os níveis de GSH e induziu as enzimas associadas à ela (GPx e GR), desencadeando diferentes respostas defensivas em cada estrutura encefálica. Portanto, os dados desta tese sugerem que a N-acetilcisteína atenua os danos oxidativos gerados pela ingestão deste edulcorante artificial. Estudos adicionais são necessários para elucidar as vias de sinalização envolvidas neste processo; bem como para determinar a quantidade dos metabólitos do aspartame (fenilalanina, aspartato e metanol) encontrada no plasma e cérebro dos ratos.Coordenação de Aperfeiçoamento de Pessoal de Nível Superior - CAPESporUniversidade Federal de Santa MariaCentro de Ciências da SaúdePrograma de Pós-Graduação em FarmacologiaUFSMBrasilFarmacologiaAttribution-NonCommercial-NoDerivatives 4.0 Internationalhttp://creativecommons.org/licenses/by-nc-nd/4.0/info:eu-repo/semantics/openAccessN-acetilcisteínaAspartameEstresse oxidativoGlutationaN-acetylcysteineOxidative stressGlutathioneCNPQ::CIENCIAS DA SAUDE::FARMACIAEfeito protetor da N-acetilcisteína sobre o estresse oxidativo causado pela administração crônica de aspartame em ratosThe protective effect of N-acetylcysteine on the oxidative stress caused by the chronic administration of aspartame in ratsinfo:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/doctoralThesisPavanato, Maria Amáliahttp://lattes.cnpq.br/8701892865724171Marroni, Norma Anair Possahttp://lattes.cnpq.br/0504456375208670Ribeiro, Maria Flavia Marqueshttp://lattes.cnpq.br/0959063179708785Leal, Daniela Bitencourt Rosahttp://lattes.cnpq.br/3639683273462361Parodi, Thaylise Veyhttp://lattes.cnpq.br/4183167775476307http://lattes.cnpq.br/9888004834158428Finamor, Isabela Andres40030000000560043a734c6-6911-4bb8-be88-cd3075162261f6afc4ba-f491-4f44-b4da-a731f912eaa0f30db17f-4339-41b0-b342-99caf3489e0d40968cfb-e3a9-4e1f-8f36-9d5d09812f6f57c82517-f994-4a9f-abc3-df1ffe4a214d1c2fb411-e1b3-4543-a5a8-1a8ad31edb06reponame:Repositório Institucional Manancial UFSMinstname:Universidade Federal de Santa Maria (UFSM)instacron:UFSMORIGINALTES_PPGFARMACOLOGIA_2015_FINAMOR_ISABELA.pdfTES_PPGFARMACOLOGIA_2015_FINAMOR_ISABELA.pdfTese de Doutoradoapplication/pdf3188003http://repositorio.ufsm.br/bitstream/1/17558/1/TES_PPGFARMACOLOGIA_2015_FINAMOR_ISABELA.pdfda66e6fa769275630de5099b7a7e3affMD51CC-LICENSElicense_rdflicense_rdfapplication/rdf+xml; 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dc.title.por.fl_str_mv |
Efeito protetor da N-acetilcisteína sobre o estresse oxidativo causado pela administração crônica de aspartame em ratos |
dc.title.alternative.eng.fl_str_mv |
The protective effect of N-acetylcysteine on the oxidative stress caused by the chronic administration of aspartame in rats |
title |
Efeito protetor da N-acetilcisteína sobre o estresse oxidativo causado pela administração crônica de aspartame em ratos |
spellingShingle |
Efeito protetor da N-acetilcisteína sobre o estresse oxidativo causado pela administração crônica de aspartame em ratos Finamor, Isabela Andres N-acetilcisteína Aspartame Estresse oxidativo Glutationa N-acetylcysteine Oxidative stress Glutathione CNPQ::CIENCIAS DA SAUDE::FARMACIA |
title_short |
Efeito protetor da N-acetilcisteína sobre o estresse oxidativo causado pela administração crônica de aspartame em ratos |
title_full |
Efeito protetor da N-acetilcisteína sobre o estresse oxidativo causado pela administração crônica de aspartame em ratos |
title_fullStr |
Efeito protetor da N-acetilcisteína sobre o estresse oxidativo causado pela administração crônica de aspartame em ratos |
title_full_unstemmed |
Efeito protetor da N-acetilcisteína sobre o estresse oxidativo causado pela administração crônica de aspartame em ratos |
title_sort |
Efeito protetor da N-acetilcisteína sobre o estresse oxidativo causado pela administração crônica de aspartame em ratos |
author |
Finamor, Isabela Andres |
author_facet |
Finamor, Isabela Andres |
author_role |
author |
dc.contributor.advisor1.fl_str_mv |
Pavanato, Maria Amália |
dc.contributor.advisor1Lattes.fl_str_mv |
http://lattes.cnpq.br/8701892865724171 |
dc.contributor.referee1.fl_str_mv |
Marroni, Norma Anair Possa |
dc.contributor.referee1Lattes.fl_str_mv |
http://lattes.cnpq.br/0504456375208670 |
dc.contributor.referee2.fl_str_mv |
Ribeiro, Maria Flavia Marques |
dc.contributor.referee2Lattes.fl_str_mv |
http://lattes.cnpq.br/0959063179708785 |
dc.contributor.referee3.fl_str_mv |
Leal, Daniela Bitencourt Rosa |
dc.contributor.referee3Lattes.fl_str_mv |
http://lattes.cnpq.br/3639683273462361 |
dc.contributor.referee4.fl_str_mv |
Parodi, Thaylise Vey |
dc.contributor.referee4Lattes.fl_str_mv |
http://lattes.cnpq.br/4183167775476307 |
dc.contributor.authorLattes.fl_str_mv |
http://lattes.cnpq.br/9888004834158428 |
dc.contributor.author.fl_str_mv |
Finamor, Isabela Andres |
contributor_str_mv |
Pavanato, Maria Amália Marroni, Norma Anair Possa Ribeiro, Maria Flavia Marques Leal, Daniela Bitencourt Rosa Parodi, Thaylise Vey |
dc.subject.por.fl_str_mv |
N-acetilcisteína Aspartame Estresse oxidativo Glutationa |
topic |
N-acetilcisteína Aspartame Estresse oxidativo Glutationa N-acetylcysteine Oxidative stress Glutathione CNPQ::CIENCIAS DA SAUDE::FARMACIA |
dc.subject.eng.fl_str_mv |
N-acetylcysteine Oxidative stress Glutathione |
dc.subject.cnpq.fl_str_mv |
CNPQ::CIENCIAS DA SAUDE::FARMACIA |
description |
This thesis evaluated the N-acetylcysteine effects (150 mg/kg, intraperitoneal) on the biochemical and oxidative changes caused by the daily oral consumption of aspartame at 40 mg/kg for six weeks by rats. For this purpose, were performed two experiments, in both the animals were divided in four groups: Control – received both aspartame and Nacetylcysteine vehicles; NAC – received aspartame vehicle, and N-acetylcysteine; ASP – received aspartame, and N-acetylcysteine vehicle; ASP-NAC – received both aspartame and N-acetylcysteine. The aspartame was administrated for six weeks; whereas the Nacetylcysteine was injected only in the fifth and sixth week. After it, the animals were anesthetized, their blood was removed, the serum was separated; and then, the rats were euthanized by exsanguination. In the first experiment, the serum was used for the measurement of glucose levels and also biomarkers of kidney and liver damage; the whole brain, liver and kidney were removed for the analysis of the oxidative stress parameters. As the results, in general, aspartame caused hyperglycemia and oxidative stress in the whole brain, and hepatic and renal tissues. N-acetylcysteine treatment protected all these tissues against the oxidative damage (lipid peroxidation and protein carbonylation), in especial, by promoting the reduced glutathione (GSH) synthesis, inducing the enzymes related to its metabolism (glutathione peroxidase (GPx), glutathione reductase (GR) and glutathione Stransferase), and elevating the ascorbic acid levels and total reactive antioxidant potential. In the second experiment, the serum was utilized for the determination of glucose content and lipid profile; the liver was removed for glucose measurement; and the whole brain was separated in the following structures: cerebral cortex, cerebellum, brainstem, and hypothalamus; in which was held the research of the oxidative stress biomarkers. The aspartame consumption caused an elevated glucose production in the liver, hyperglycemia, hypertriglyceridemia, hypercholesterolemia; and oxidative stress in all the brain regions. Although N-acetylcysteine treatment did not reduce neither the synthesis of liver glucose nor the hyperglycemia, it normalized the triglycerides and high-density lipoprotein cholesterol in the serum. This antioxidative treatment also protected all the brain regions against the lipid peroxidation, increased GSH levels and induced its associated enzymes (GPx and GR), triggering different defensive responses according each brain region. Therefore, the data of this thesis suggest that N-acetylcysteine attenuates the oxidative damage generated by the intake of this artificial sweetener. More studies were needed to elucidate the signaling pathways involved in this process; as well as to determine the aspartame metabolites levels (phenylalanine, aspartate and methanol) found in the rat plasma and brain. |
publishDate |
2015 |
dc.date.issued.fl_str_mv |
2015-03-12 |
dc.date.accessioned.fl_str_mv |
2019-07-25T17:35:24Z |
dc.date.available.fl_str_mv |
2019-07-25T17:35:24Z |
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/1/17558 |
url |
http://repositorio.ufsm.br/handle/1/17558 |
dc.language.iso.fl_str_mv |
por |
language |
por |
dc.relation.cnpq.fl_str_mv |
400300000005 |
dc.relation.confidence.fl_str_mv |
600 |
dc.relation.authority.fl_str_mv |
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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 da Saúde |
dc.publisher.program.fl_str_mv |
Programa de Pós-Graduação em Farmacologia |
dc.publisher.initials.fl_str_mv |
UFSM |
dc.publisher.country.fl_str_mv |
Brasil |
dc.publisher.department.fl_str_mv |
Farmacologia |
publisher.none.fl_str_mv |
Universidade Federal de Santa Maria Centro de Ciências da Saúde |
dc.source.none.fl_str_mv |
reponame:Repositório Institucional Manancial 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 |
Repositório Institucional Manancial UFSM |
collection |
Repositório Institucional Manancial UFSM |
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MD5 MD5 MD5 MD5 MD5 |
repository.name.fl_str_mv |
Repositório Institucional Manancial UFSM - Universidade Federal de Santa Maria (UFSM) |
repository.mail.fl_str_mv |
ouvidoria@ufsm.br |
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1808854730303078400 |