Influência da periodontite apical sobre parâmetros de estresse oxidativo e atividades de ATPases em diferentes órgãos de ratos adultos e jovens
Autor(a) principal: | |
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Data de Publicação: | 2020 |
Tipo de documento: | Tese |
Idioma: | por |
Título da fonte: | Repositório Institucional Manancial UFSM |
Texto Completo: | http://repositorio.ufsm.br/handle/1/22154 |
Resumo: | Apical periodontitis, inflammatory process around the apex of a tooth root, is primarily a sequel to microbial infection of the pulp space of teeth and is a remarkably widespread problem. P-type ATPases, as Na+/K+-ATPase (NKA) and Ca2+-ATPase (CAA), create electrochemical potential gradients for the different ions essential for various cellular functions. Such transmembrane enzymes have an oxidative regulation and are associated with the pathogenesis of various systemic diseases. However, its relationship with apical periodontitis has not yet been reported. Considering that oxidative stress is related to the pathogenesis of apical periodontitis, this study was designed to evaluate the influence of apical periodontitis on oxidative stress parameters and ATPases activities in different organs of adult and young rats. Adult male Wistar rats were randomly assigned to two experimental groups: control (CT; no periapical lesion; n=8) and apical periodontitis (AP; with apical periodontitis; n=9). Apical periodontitis was induced by pulpal exposure of the right mandibular first molar. After 21 days of apical periodontitis induction, the rats were euthanized and the jaws dissected for radiographic and histological analysis. In addition, the heart, liver, pancreas and kidneys were collected for biochemical analyzes of NKA activity, reactive species (RS) generation and endogenous antioxidant content. Apical periodontitis increased NKA activity in the heart, liver and pancreas; increased RS generation only in the heart. However, the same influence was not observed in the kidney. While in the heart and pancreas was observed a reduction in endogenous antioxidant defenses, in the liver and kidney such levels were increased. NKA activity and endogenous antioxidant defense system modulations observed in this study suggest that alteration of cellular electrochemical gradient and antioxidant status may be involved in the pathophysiology of apical periodontitis. To continue the studies, to verify if there is influence of age and different pulp exposure times on the same parameters analyzed, a second experimental protocol was developed with young male Wistar rats that were also randomly assigned to two experimental groups: control (CT; no apical periodontitis; n = 21) and apical periodontitis (AP; with apical periodontitis; n = 24). Apical periodontitis was induced by pulpal exposure of the right mandibular first molar. After 7, 14 and 21 days of apical periodontitis induction, the rats were euthanized and the mandibles were dissected for radiographic analysis. In addition, the heart, liver, pancreas and kidney were collected for biochemical analyzes of the RS generation, levels of the lipoperoxidation and protein carbonyls, besides NKA and CAA activities. Apical periodontitis induced oxidative damage to the heart, liver and pancreas, observed mainly 21 days after pulp exposure. In addition, apical periodontitis was related to reduced activities in NAK and CAA in all organs analyzed, except the pancreas, in which an increase in CAA activity was observed at all times evaluated. The reduction in the activity of NKA and CAA, the modulation of the endogenous antioxidant defense system and the increase in oxidative damage observed in this study suggest that changes in the cellular electrochemical gradient and oxidative stress may be involved in the pathophysiology of apical periodontitis. |
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2021-09-03T18:25:16Z2021-09-03T18:25:16Z2020-04-17http://repositorio.ufsm.br/handle/1/22154Apical periodontitis, inflammatory process around the apex of a tooth root, is primarily a sequel to microbial infection of the pulp space of teeth and is a remarkably widespread problem. P-type ATPases, as Na+/K+-ATPase (NKA) and Ca2+-ATPase (CAA), create electrochemical potential gradients for the different ions essential for various cellular functions. Such transmembrane enzymes have an oxidative regulation and are associated with the pathogenesis of various systemic diseases. However, its relationship with apical periodontitis has not yet been reported. Considering that oxidative stress is related to the pathogenesis of apical periodontitis, this study was designed to evaluate the influence of apical periodontitis on oxidative stress parameters and ATPases activities in different organs of adult and young rats. Adult male Wistar rats were randomly assigned to two experimental groups: control (CT; no periapical lesion; n=8) and apical periodontitis (AP; with apical periodontitis; n=9). Apical periodontitis was induced by pulpal exposure of the right mandibular first molar. After 21 days of apical periodontitis induction, the rats were euthanized and the jaws dissected for radiographic and histological analysis. In addition, the heart, liver, pancreas and kidneys were collected for biochemical analyzes of NKA activity, reactive species (RS) generation and endogenous antioxidant content. Apical periodontitis increased NKA activity in the heart, liver and pancreas; increased RS generation only in the heart. However, the same influence was not observed in the kidney. While in the heart and pancreas was observed a reduction in endogenous antioxidant defenses, in the liver and kidney such levels were increased. NKA activity and endogenous antioxidant defense system modulations observed in this study suggest that alteration of cellular electrochemical gradient and antioxidant status may be involved in the pathophysiology of apical periodontitis. To continue the studies, to verify if there is influence of age and different pulp exposure times on the same parameters analyzed, a second experimental protocol was developed with young male Wistar rats that were also randomly assigned to two experimental groups: control (CT; no apical periodontitis; n = 21) and apical periodontitis (AP; with apical periodontitis; n = 24). Apical periodontitis was induced by pulpal exposure of the right mandibular first molar. After 7, 14 and 21 days of apical periodontitis induction, the rats were euthanized and the mandibles were dissected for radiographic analysis. In addition, the heart, liver, pancreas and kidney were collected for biochemical analyzes of the RS generation, levels of the lipoperoxidation and protein carbonyls, besides NKA and CAA activities. Apical periodontitis induced oxidative damage to the heart, liver and pancreas, observed mainly 21 days after pulp exposure. In addition, apical periodontitis was related to reduced activities in NAK and CAA in all organs analyzed, except the pancreas, in which an increase in CAA activity was observed at all times evaluated. The reduction in the activity of NKA and CAA, the modulation of the endogenous antioxidant defense system and the increase in oxidative damage observed in this study suggest that changes in the cellular electrochemical gradient and oxidative stress may be involved in the pathophysiology of apical periodontitis.A periodontite apical, processo inflamatório em torno do ápice da raiz de um dente, é uma sequela da infecção microbiana do espaço pulpar dos dentes e é um problema notavelmente disseminado. ATPases do tipo P, como a Na+/K+-ATPase (NKA) e a Ca2+-ATPase (CAA), criam gradientes de potencial eletroquímico para os diferentes íons essenciais para diversas funções celulares, variando desde a geração de potencial de membrana, até contração muscular e remoção de íons tóxicos das células. Tais enzimas transmembranares possuem uma regulação oxidativa e estão associadas à patogênese de várias doenças sistêmicas, como obesidade, diabetes, dislipidemia e aterosclerose. No entanto, sua relação com a periodontite apical ainda não foi relatada. Considerando que o estresse oxidativo está relacionado à patogênese da periodontite apical, este estudo foi desenvolvido para avaliar a influência da periodontite apical sobre parâmetros de estresse oxidativo e atividades d ATPases em diferentes órgãos de ratos adultos e jovens. Ratos Wistar machos adultos foram aleatoriamente designados a dois grupos experimentais: controle (CT; sem lesão periapical; n=8) e periodontite apical (AP; com periodontite apical; n=9). A periodontite apical foi induzida pela exposição pulpar do primeiro molar mandibular direito. Após 21 dias da indução da periodontite apical, os animais foram eutanasiados e as mandíbulas foram dissecadas para as análises radiográfica e histológica. Além disso, o coração, fígado, pâncreas e rins foram coletados para as análises bioquímicas da atividade da NKA, geração de espécies reativas (ER) e conteúdo de antioxidantes endógenos. A periodontite apical aumentou a atividade da NKA no coração, fígado e pâncreas; e aumentou a geração dos ER apenas no coração. No entanto, a mesma influência não foi observada nos rim. Enquanto no coração e no pâncreas foi observado uma redução das defesas antioxidantes endógenas, no fígado e no rim tais níveis foram aumentados. Na continuidade dos estudos, para verificar se existe influência da idade e de diferentes tempos de exposição pulpar sobre os mesmos parâmetros analisados, um segundo protocolo experimental foi desenvolvido com ratos Wistar machos jovens que foram também aleatoriamente designados a dois grupos experimentais: controle (CT; sem periodontite apical; n=21) e periodontite apical (PA; com periodontite apical; n=24). A periodontite apical foi induzida pela exposição pulpar do primeiro molar mandibular direito. Após 7, 14 e 21 dias da indução da periodontite apical, os ratos foram eutanasiados e as mandíbulas foram dissecadas para análise radiográfica. Além disso, o coração, fígado e o pâncreas foram coletados para as análises bioquímicas da geração de ER, níveis de lipoperoxidação e de carbonilação de proteínas, além das atividades da NKA e da CAA. A periodontite apical induziu danos oxidativos no coração, fígado e pâncreas, observados principalmente 21 dias após a exposição pulpar. Além disso, a periodontite apical foi relacionada à redução das atividades na NAK e da CAA em todos os órgãos analisados, exceto no pâncreas, no qual se observou um aumento na atividade da CAA em todos os tempos avaliados. A redução da atividade da NKA e da CAA, a modulação do sistema de defesa antioxidante endógeno e o aumento dos danos oxidativos observados nesse estudo sugerem que a alteração do gradiente eletroquímico celular e o estresse oxidativo podem estar envolvidos na fisiopatologia da periodontite apical.porUniversidade Federal de Santa MariaCentro de Ciências da SaúdePrograma de Pós-Graduação em Ciências OdontológicasUFSMBrasilOdontologiaAttribution-NonCommercial-NoDerivatives 4.0 Internationalhttp://creativecommons.org/licenses/by-nc-nd/4.0/info:eu-repo/semantics/openAccessLesão periapicalBomba de cálcioBomba de sódioSistema de defesa antioxidantePeriapical lesionCalcium pumpSodium pumpAntioxidant defense systemCNPQ::CIENCIAS DA SAUDE::ODONTOLOGIAInfluência da periodontite apical sobre parâmetros de estresse oxidativo e atividades de ATPases em diferentes órgãos de ratos adultos e jovensInfluence of apical periodontitis on oxidative stress parameters and Na+K+-ATPase and Ca2+-ATPase activities in different stages of rat developmentinfo:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/doctoralThesisBier, Carlos Alexandre Souzahttp://lattes.cnpq.br/6734133387557316Bürger, Marilise EscobarWolle, Carlos Frederico BrilhanteBenvegnú, Dalila MoterPappen, Fernanda GeraldoSegat, Hecson Jesserhttp://lattes.cnpq.br/3355023039056051Barcelos, Raquel Cristine Silva4002000000006006006006006006006b1a86d0-0227-4255-bfc5-df7b3c0ba88726732b56-6ba3-4587-93a9-1c90f032a796e414b039-9548-413f-9c3a-887aebf85334eb48493f-8180-4efb-a475-4def95146d8ffcf10e76-96ec-4734-88db-458167adfddd52e2acb4-392a-4cc3-a88f-b1e861ab768d3d385389-1d0a-4c62-bae1-1f7fa97480a7reponame:Repositório Institucional Manancial UFSMinstname:Universidade Federal de Santa Maria (UFSM)instacron:UFSMORIGINALTES_PPGCO_2020_BARCELOS_RAQUEL.pdfTES_PPGCO_2020_BARCELOS_RAQUEL.pdfTese de Doutoradoapplication/pdf1463339http://repositorio.ufsm.br/bitstream/1/22154/1/TES_PPGCO_2020_BARCELOS_RAQUEL.pdf0bf2cecd88115db689bb487c73cc4466MD51CC-LICENSElicense_rdflicense_rdfapplication/rdf+xml; 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dc.title.por.fl_str_mv |
Influência da periodontite apical sobre parâmetros de estresse oxidativo e atividades de ATPases em diferentes órgãos de ratos adultos e jovens |
dc.title.alternative.eng.fl_str_mv |
Influence of apical periodontitis on oxidative stress parameters and Na+K+-ATPase and Ca2+-ATPase activities in different stages of rat development |
title |
Influência da periodontite apical sobre parâmetros de estresse oxidativo e atividades de ATPases em diferentes órgãos de ratos adultos e jovens |
spellingShingle |
Influência da periodontite apical sobre parâmetros de estresse oxidativo e atividades de ATPases em diferentes órgãos de ratos adultos e jovens Barcelos, Raquel Cristine Silva Lesão periapical Bomba de cálcio Bomba de sódio Sistema de defesa antioxidante Periapical lesion Calcium pump Sodium pump Antioxidant defense system CNPQ::CIENCIAS DA SAUDE::ODONTOLOGIA |
title_short |
Influência da periodontite apical sobre parâmetros de estresse oxidativo e atividades de ATPases em diferentes órgãos de ratos adultos e jovens |
title_full |
Influência da periodontite apical sobre parâmetros de estresse oxidativo e atividades de ATPases em diferentes órgãos de ratos adultos e jovens |
title_fullStr |
Influência da periodontite apical sobre parâmetros de estresse oxidativo e atividades de ATPases em diferentes órgãos de ratos adultos e jovens |
title_full_unstemmed |
Influência da periodontite apical sobre parâmetros de estresse oxidativo e atividades de ATPases em diferentes órgãos de ratos adultos e jovens |
title_sort |
Influência da periodontite apical sobre parâmetros de estresse oxidativo e atividades de ATPases em diferentes órgãos de ratos adultos e jovens |
author |
Barcelos, Raquel Cristine Silva |
author_facet |
Barcelos, Raquel Cristine Silva |
author_role |
author |
dc.contributor.advisor1.fl_str_mv |
Bier, Carlos Alexandre Souza |
dc.contributor.advisor1Lattes.fl_str_mv |
http://lattes.cnpq.br/6734133387557316 |
dc.contributor.advisor-co1.fl_str_mv |
Bürger, Marilise Escobar |
dc.contributor.referee1.fl_str_mv |
Wolle, Carlos Frederico Brilhante |
dc.contributor.referee2.fl_str_mv |
Benvegnú, Dalila Moter |
dc.contributor.referee3.fl_str_mv |
Pappen, Fernanda Geraldo |
dc.contributor.referee4.fl_str_mv |
Segat, Hecson Jesser |
dc.contributor.authorLattes.fl_str_mv |
http://lattes.cnpq.br/3355023039056051 |
dc.contributor.author.fl_str_mv |
Barcelos, Raquel Cristine Silva |
contributor_str_mv |
Bier, Carlos Alexandre Souza Bürger, Marilise Escobar Wolle, Carlos Frederico Brilhante Benvegnú, Dalila Moter Pappen, Fernanda Geraldo Segat, Hecson Jesser |
dc.subject.por.fl_str_mv |
Lesão periapical Bomba de cálcio Bomba de sódio Sistema de defesa antioxidante |
topic |
Lesão periapical Bomba de cálcio Bomba de sódio Sistema de defesa antioxidante Periapical lesion Calcium pump Sodium pump Antioxidant defense system CNPQ::CIENCIAS DA SAUDE::ODONTOLOGIA |
dc.subject.eng.fl_str_mv |
Periapical lesion Calcium pump Sodium pump Antioxidant defense system |
dc.subject.cnpq.fl_str_mv |
CNPQ::CIENCIAS DA SAUDE::ODONTOLOGIA |
description |
Apical periodontitis, inflammatory process around the apex of a tooth root, is primarily a sequel to microbial infection of the pulp space of teeth and is a remarkably widespread problem. P-type ATPases, as Na+/K+-ATPase (NKA) and Ca2+-ATPase (CAA), create electrochemical potential gradients for the different ions essential for various cellular functions. Such transmembrane enzymes have an oxidative regulation and are associated with the pathogenesis of various systemic diseases. However, its relationship with apical periodontitis has not yet been reported. Considering that oxidative stress is related to the pathogenesis of apical periodontitis, this study was designed to evaluate the influence of apical periodontitis on oxidative stress parameters and ATPases activities in different organs of adult and young rats. Adult male Wistar rats were randomly assigned to two experimental groups: control (CT; no periapical lesion; n=8) and apical periodontitis (AP; with apical periodontitis; n=9). Apical periodontitis was induced by pulpal exposure of the right mandibular first molar. After 21 days of apical periodontitis induction, the rats were euthanized and the jaws dissected for radiographic and histological analysis. In addition, the heart, liver, pancreas and kidneys were collected for biochemical analyzes of NKA activity, reactive species (RS) generation and endogenous antioxidant content. Apical periodontitis increased NKA activity in the heart, liver and pancreas; increased RS generation only in the heart. However, the same influence was not observed in the kidney. While in the heart and pancreas was observed a reduction in endogenous antioxidant defenses, in the liver and kidney such levels were increased. NKA activity and endogenous antioxidant defense system modulations observed in this study suggest that alteration of cellular electrochemical gradient and antioxidant status may be involved in the pathophysiology of apical periodontitis. To continue the studies, to verify if there is influence of age and different pulp exposure times on the same parameters analyzed, a second experimental protocol was developed with young male Wistar rats that were also randomly assigned to two experimental groups: control (CT; no apical periodontitis; n = 21) and apical periodontitis (AP; with apical periodontitis; n = 24). Apical periodontitis was induced by pulpal exposure of the right mandibular first molar. After 7, 14 and 21 days of apical periodontitis induction, the rats were euthanized and the mandibles were dissected for radiographic analysis. In addition, the heart, liver, pancreas and kidney were collected for biochemical analyzes of the RS generation, levels of the lipoperoxidation and protein carbonyls, besides NKA and CAA activities. Apical periodontitis induced oxidative damage to the heart, liver and pancreas, observed mainly 21 days after pulp exposure. In addition, apical periodontitis was related to reduced activities in NAK and CAA in all organs analyzed, except the pancreas, in which an increase in CAA activity was observed at all times evaluated. The reduction in the activity of NKA and CAA, the modulation of the endogenous antioxidant defense system and the increase in oxidative damage observed in this study suggest that changes in the cellular electrochemical gradient and oxidative stress may be involved in the pathophysiology of apical periodontitis. |
publishDate |
2020 |
dc.date.issued.fl_str_mv |
2020-04-17 |
dc.date.accessioned.fl_str_mv |
2021-09-03T18:25:16Z |
dc.date.available.fl_str_mv |
2021-09-03T18:25:16Z |
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/1/22154 |
url |
http://repositorio.ufsm.br/handle/1/22154 |
dc.language.iso.fl_str_mv |
por |
language |
por |
dc.relation.cnpq.fl_str_mv |
400200000000 |
dc.relation.confidence.fl_str_mv |
600 600 600 600 600 600 |
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 Ciências Odontológicas |
dc.publisher.initials.fl_str_mv |
UFSM |
dc.publisher.country.fl_str_mv |
Brasil |
dc.publisher.department.fl_str_mv |
Odontologia |
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 |
bitstream.url.fl_str_mv |
http://repositorio.ufsm.br/bitstream/1/22154/1/TES_PPGCO_2020_BARCELOS_RAQUEL.pdf http://repositorio.ufsm.br/bitstream/1/22154/2/license_rdf http://repositorio.ufsm.br/bitstream/1/22154/3/license.txt http://repositorio.ufsm.br/bitstream/1/22154/4/TES_PPGCO_2020_BARCELOS_RAQUEL.pdf.txt http://repositorio.ufsm.br/bitstream/1/22154/5/TES_PPGCO_2020_BARCELOS_RAQUEL.pdf.jpg |
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bitstream.checksumAlgorithm.fl_str_mv |
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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1808854720248283136 |