Lipid damage is the best marker of oxidative injury during the cardiac remodeling process induced by tobacco smoke
Autor(a) principal: | |
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Data de Publicação: | 2018 |
Outros Autores: | , , , , , , , , , , , , |
Tipo de documento: | Artigo |
Idioma: | eng |
Título da fonte: | Repositório Institucional da UNESP |
Texto Completo: | http://dx.doi.org/10.1186/s40360-018-0268-4 http://hdl.handle.net/11449/188374 |
Resumo: | BACKGROUND: Oxidative stress is one potential mechanism that explain the direct effects of smoking on cardiac remodeling process. However, no study has compared different myocardial products of macromolecule oxidation after tobacco smoke exposure. Thus, the aim of this study was to investigate the lipid hydroperoxide (LH) levels, protein carbonyl concentrations and DNA damage in cardiac tissue of rats exposed to tobacco smoke. METHODS: Male Wistar rats were divided into two groups: group C (control, n = 14) composed of animals not exposed to cigarette smoke; group ETS (exposed to tobacco smoke, n = 14) composed by animals exposed to cigarette smoke. The animals were exposed to 2 month of ETS and morphological, biochemical and functional analyses were performed. RESULTS: Cardiac cotinine levels were elevated in the ETS group. In addition, the myocyte cross-sectional area was higher in the ETS group. (C = 266.6 ± 23.2 μm2 and ETS = 347.5 ± 15.1 μm2, p < 0.001). Cardiac LH was higher in the ETS group than in group C (C = 196.4 ± 51.5 nmol/g and ETS = 331.9 ± 52.9 nmol/g, p < 0.001). However, there were no between-group differences in cardiac protein carbonyl concentration or DNA damage. CONCLUSIONS: Therefore, our results suggest that, in this model, lipid damage is a good marker of oxidative damage during the cardiac remodeling process induced by 2 months of exposure to tobacco smoke. |
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Lipid damage is the best marker of oxidative injury during the cardiac remodeling process induced by tobacco smokeCigarette smokeComet assayDNA damageProtein carbonyl groupsBACKGROUND: Oxidative stress is one potential mechanism that explain the direct effects of smoking on cardiac remodeling process. However, no study has compared different myocardial products of macromolecule oxidation after tobacco smoke exposure. Thus, the aim of this study was to investigate the lipid hydroperoxide (LH) levels, protein carbonyl concentrations and DNA damage in cardiac tissue of rats exposed to tobacco smoke. METHODS: Male Wistar rats were divided into two groups: group C (control, n = 14) composed of animals not exposed to cigarette smoke; group ETS (exposed to tobacco smoke, n = 14) composed by animals exposed to cigarette smoke. The animals were exposed to 2 month of ETS and morphological, biochemical and functional analyses were performed. RESULTS: Cardiac cotinine levels were elevated in the ETS group. In addition, the myocyte cross-sectional area was higher in the ETS group. (C = 266.6 ± 23.2 μm2 and ETS = 347.5 ± 15.1 μm2, p < 0.001). Cardiac LH was higher in the ETS group than in group C (C = 196.4 ± 51.5 nmol/g and ETS = 331.9 ± 52.9 nmol/g, p < 0.001). However, there were no between-group differences in cardiac protein carbonyl concentration or DNA damage. CONCLUSIONS: Therefore, our results suggest that, in this model, lipid damage is a good marker of oxidative damage during the cardiac remodeling process induced by 2 months of exposure to tobacco smoke.Internal Medicine Department Botucatu Medical School UNESP - São Paulo State UniversityDepartment of Anesthesiology Botucatu Medical School UNESP - São Paulo State UniversityDepartment of Genetics Institute of Biological Sciences UNESP - São Paulo State UniversityChemistry and Biochemistry Department Institute of Biological Sciences Botucatu Medical School UNESP - São Paulo State UniversityDepartamento de Clínica Médica Faculdade de Medicina de Botucatu 18618-000, Rubião Júnior s/nInternal Medicine Department Botucatu Medical School UNESP - São Paulo State UniversityDepartment of Anesthesiology Botucatu Medical School UNESP - São Paulo State UniversityDepartment of Genetics Institute of Biological Sciences UNESP - São Paulo State UniversityChemistry and Biochemistry Department Institute of Biological Sciences Botucatu Medical School UNESP - São Paulo State UniversityDepartamento de Clínica Médica Faculdade de Medicina de Botucatu 18618-000, Rubião Júnior s/nUniversidade Estadual Paulista (Unesp)Lourenço, Maria Angélica Martins [UNESP]Braz, Mariana Gobbo [UNESP]Aun, Aline Garcia [UNESP]Pereira, Bruna Letícia Buzati [UNESP]Fernandes, Fábio Henrique [UNESP]Kazmarek, Elisa Moya [UNESP]Bachiega, Tatiana Fernanda [UNESP]Zanati, Silmeia Garcia [UNESP]Azevedo, Paula Schmidt [UNESP]Polegato, Bertha Furlan [UNESP]Fernandes, Ana Angélica Henrique [UNESP]de Paiva, Sergio Alberto Rupp [UNESP]Zornoff, Leonardo Antonio Mamede [UNESP]Minicucci, Marcos Ferreira [UNESP]2019-10-06T16:06:02Z2019-10-06T16:06:02Z2018-11-16info:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/article74http://dx.doi.org/10.1186/s40360-018-0268-4BMC pharmacology & toxicology, v. 19, n. 1, p. 74-, 2018.2050-6511http://hdl.handle.net/11449/18837410.1186/s40360-018-0268-42-s2.0-8505672427050168390153945471213140801402647743870403447167355300230102038040000-0002-5843-6232Scopusreponame:Repositório Institucional da UNESPinstname:Universidade Estadual Paulista (UNESP)instacron:UNESPengBMC pharmacology & toxicologyinfo:eu-repo/semantics/openAccess2021-10-23T21:47:18Zoai:repositorio.unesp.br:11449/188374Repositório InstitucionalPUBhttp://repositorio.unesp.br/oai/requestopendoar:29462021-10-23T21:47:18Repositório Institucional da UNESP - Universidade Estadual Paulista (UNESP)false |
dc.title.none.fl_str_mv |
Lipid damage is the best marker of oxidative injury during the cardiac remodeling process induced by tobacco smoke |
title |
Lipid damage is the best marker of oxidative injury during the cardiac remodeling process induced by tobacco smoke |
spellingShingle |
Lipid damage is the best marker of oxidative injury during the cardiac remodeling process induced by tobacco smoke Lourenço, Maria Angélica Martins [UNESP] Cigarette smoke Comet assay DNA damage Protein carbonyl groups |
title_short |
Lipid damage is the best marker of oxidative injury during the cardiac remodeling process induced by tobacco smoke |
title_full |
Lipid damage is the best marker of oxidative injury during the cardiac remodeling process induced by tobacco smoke |
title_fullStr |
Lipid damage is the best marker of oxidative injury during the cardiac remodeling process induced by tobacco smoke |
title_full_unstemmed |
Lipid damage is the best marker of oxidative injury during the cardiac remodeling process induced by tobacco smoke |
title_sort |
Lipid damage is the best marker of oxidative injury during the cardiac remodeling process induced by tobacco smoke |
author |
Lourenço, Maria Angélica Martins [UNESP] |
author_facet |
Lourenço, Maria Angélica Martins [UNESP] Braz, Mariana Gobbo [UNESP] Aun, Aline Garcia [UNESP] Pereira, Bruna Letícia Buzati [UNESP] Fernandes, Fábio Henrique [UNESP] Kazmarek, Elisa Moya [UNESP] Bachiega, Tatiana Fernanda [UNESP] Zanati, Silmeia Garcia [UNESP] Azevedo, Paula Schmidt [UNESP] Polegato, Bertha Furlan [UNESP] Fernandes, Ana Angélica Henrique [UNESP] de Paiva, Sergio Alberto Rupp [UNESP] Zornoff, Leonardo Antonio Mamede [UNESP] Minicucci, Marcos Ferreira [UNESP] |
author_role |
author |
author2 |
Braz, Mariana Gobbo [UNESP] Aun, Aline Garcia [UNESP] Pereira, Bruna Letícia Buzati [UNESP] Fernandes, Fábio Henrique [UNESP] Kazmarek, Elisa Moya [UNESP] Bachiega, Tatiana Fernanda [UNESP] Zanati, Silmeia Garcia [UNESP] Azevedo, Paula Schmidt [UNESP] Polegato, Bertha Furlan [UNESP] Fernandes, Ana Angélica Henrique [UNESP] de Paiva, Sergio Alberto Rupp [UNESP] Zornoff, Leonardo Antonio Mamede [UNESP] Minicucci, Marcos Ferreira [UNESP] |
author2_role |
author author author author author author author author author author author author author |
dc.contributor.none.fl_str_mv |
Universidade Estadual Paulista (Unesp) |
dc.contributor.author.fl_str_mv |
Lourenço, Maria Angélica Martins [UNESP] Braz, Mariana Gobbo [UNESP] Aun, Aline Garcia [UNESP] Pereira, Bruna Letícia Buzati [UNESP] Fernandes, Fábio Henrique [UNESP] Kazmarek, Elisa Moya [UNESP] Bachiega, Tatiana Fernanda [UNESP] Zanati, Silmeia Garcia [UNESP] Azevedo, Paula Schmidt [UNESP] Polegato, Bertha Furlan [UNESP] Fernandes, Ana Angélica Henrique [UNESP] de Paiva, Sergio Alberto Rupp [UNESP] Zornoff, Leonardo Antonio Mamede [UNESP] Minicucci, Marcos Ferreira [UNESP] |
dc.subject.por.fl_str_mv |
Cigarette smoke Comet assay DNA damage Protein carbonyl groups |
topic |
Cigarette smoke Comet assay DNA damage Protein carbonyl groups |
description |
BACKGROUND: Oxidative stress is one potential mechanism that explain the direct effects of smoking on cardiac remodeling process. However, no study has compared different myocardial products of macromolecule oxidation after tobacco smoke exposure. Thus, the aim of this study was to investigate the lipid hydroperoxide (LH) levels, protein carbonyl concentrations and DNA damage in cardiac tissue of rats exposed to tobacco smoke. METHODS: Male Wistar rats were divided into two groups: group C (control, n = 14) composed of animals not exposed to cigarette smoke; group ETS (exposed to tobacco smoke, n = 14) composed by animals exposed to cigarette smoke. The animals were exposed to 2 month of ETS and morphological, biochemical and functional analyses were performed. RESULTS: Cardiac cotinine levels were elevated in the ETS group. In addition, the myocyte cross-sectional area was higher in the ETS group. (C = 266.6 ± 23.2 μm2 and ETS = 347.5 ± 15.1 μm2, p < 0.001). Cardiac LH was higher in the ETS group than in group C (C = 196.4 ± 51.5 nmol/g and ETS = 331.9 ± 52.9 nmol/g, p < 0.001). However, there were no between-group differences in cardiac protein carbonyl concentration or DNA damage. CONCLUSIONS: Therefore, our results suggest that, in this model, lipid damage is a good marker of oxidative damage during the cardiac remodeling process induced by 2 months of exposure to tobacco smoke. |
publishDate |
2018 |
dc.date.none.fl_str_mv |
2018-11-16 2019-10-06T16:06:02Z 2019-10-06T16:06:02Z |
dc.type.status.fl_str_mv |
info:eu-repo/semantics/publishedVersion |
dc.type.driver.fl_str_mv |
info:eu-repo/semantics/article |
format |
article |
status_str |
publishedVersion |
dc.identifier.uri.fl_str_mv |
http://dx.doi.org/10.1186/s40360-018-0268-4 BMC pharmacology & toxicology, v. 19, n. 1, p. 74-, 2018. 2050-6511 http://hdl.handle.net/11449/188374 10.1186/s40360-018-0268-4 2-s2.0-85056724270 5016839015394547 1213140801402647 7438704034471673 5530023010203804 0000-0002-5843-6232 |
url |
http://dx.doi.org/10.1186/s40360-018-0268-4 http://hdl.handle.net/11449/188374 |
identifier_str_mv |
BMC pharmacology & toxicology, v. 19, n. 1, p. 74-, 2018. 2050-6511 10.1186/s40360-018-0268-4 2-s2.0-85056724270 5016839015394547 1213140801402647 7438704034471673 5530023010203804 0000-0002-5843-6232 |
dc.language.iso.fl_str_mv |
eng |
language |
eng |
dc.relation.none.fl_str_mv |
BMC pharmacology & toxicology |
dc.rights.driver.fl_str_mv |
info:eu-repo/semantics/openAccess |
eu_rights_str_mv |
openAccess |
dc.format.none.fl_str_mv |
74 |
dc.source.none.fl_str_mv |
Scopus reponame:Repositório Institucional da UNESP instname:Universidade Estadual Paulista (UNESP) instacron:UNESP |
instname_str |
Universidade Estadual Paulista (UNESP) |
instacron_str |
UNESP |
institution |
UNESP |
reponame_str |
Repositório Institucional da UNESP |
collection |
Repositório Institucional da UNESP |
repository.name.fl_str_mv |
Repositório Institucional da UNESP - Universidade Estadual Paulista (UNESP) |
repository.mail.fl_str_mv |
|
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1799965300923301888 |