Efeitos da administração de beta-bloqueador na remodelação ventricular induzida pelo tabagismo em ratos

Duarte, Delfim; Oliveira, Lucienne C.; Minicucci, Marcos F.; Azevedo, Paulo Furquim de; Matsubara, Beatriz Bojikian; Matsubara, Luiz Shiguero; Campana, Álvaro Oscar; Paiva, Sérgio Alberto Rupp de; Zornoff, Leonardo A. M.

doi:10.1590/s0066-782x2009000600011

Cited by 7 publications

(4 citation statements)

References 29 publications

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“…Therefore, isolated heart preparation permits the analysis of cardiac function without interference of confounding variables, such as neurohormonal and hemodynamic factors. In this model, ETS induced hemodynamic alterations [ 35 , 36 ]. Additionally, the cardiac remodeling and increased blood pressure induced by ETS were attenuated by lisinopril or propranolol [ 35 , 36 ].…”

Section: Discussionmentioning

confidence: 99%

“…In this model, ETS induced hemodynamic alterations [ 35 , 36 ]. Additionally, the cardiac remodeling and increased blood pressure induced by ETS were attenuated by lisinopril or propranolol [ 35 , 36 ]. Therefore, the contradictory results of the in vivo and in vitro functional analyses reinforce the importance of neurohormonal/hemodynamic changes in the remodeling process induced by ETS.…”

Section: Discussionmentioning

confidence: 99%

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Lipid damage is the best marker of oxidative injury during the cardiac remodeling process induced by tobacco smoke

Lourenço

Braz

Aun

et al. 2018

BMC Pharmacol Toxicol

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BackgroundOxidative 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.MethodsMale 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.ResultsCardiac 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.ConclusionsTherefore, 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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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Lipid damage is the best marker of oxidative injury during the cardiac remodeling process induced by tobacco smoke

Lourenço

Braz

Aun

et al. 2018

BMC Pharmacol Toxicol

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“…Finalmente, o uso de propranolol e lisinopril atenuou a remodelação induzida pelo fumo, sugerindo que os sistemas simpático e renina-angiotensina participam das alterações cardíacas induzidas pela exposição à fumaça do cigarro (15,49) . (63) .…”

Section: Tabela 6 -Distribuição Das Isoformas Das Cadeias Pesadas Da unclassified

“…Acompanhando essas alterações, o tabagismo resulta em queda de parâmetros de função sistólica e diastólica, tanto in vivo, como in vitro. Sendo assim, evidências sugerem que a exposição ao fumo pode modular o processo de remodelação ventricular (11,12,13,14,15) .…”

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Influência da taurina na remodelação cardíaca induzida pela exposição à fumaça do cigarro

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Effect of Second-Hand Tobacco Smoke on the Nitration of Brain Proteins: A Systems Biology and Bioinformatics Approach

Kobeissy

Guingab‐Cagmat

Bruijnzeel

et al. 2017

Methods in Molecular Biology

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Second-hand smoke (SHS) exposure leads to the death of approximately 48,000 nonsmokers per year in the United States alone. SHS exposure has been associated with cardiovascular, respiratory, and neurodegenerative diseases. While cardiac function abnormalities and lung cancer due to SHS have been well characterized, brain injury due to SHS has not undergone a full systematic evaluation. Oxidative stress and nitration have been associated with smoking and SHS exposure. Animal studies suggest that exposure to tobacco smoke increases oxidative stress. Oxidative stress is characterized by an increase in reactive oxygen and nitrogen species (ROS/RNS). Among the oxidative mechanisms affecting protein functionality is the posttranslational modification (PTM)-mediated tyrosine nitration. Protein tyrosine nitration, a covalent posttranslational modification, is commonly used as a marker of cellular oxidative stress associated with the pathogenesis of several neurodegenerative diseases. In our previous published work, the utility of a targeted proteomic approach has been evaluated to identify two brain abundant proteins in an in vivo SHS rat model namely the GAPDH and UCH-L1. In this current study, mass spectrometric-based proteomic and complementary biochemical methods were used to characterize the SHS-induced brain nitroproteome followed by bioinformatics/systems biology approach analysis to characterize protein interaction map. Sprague Dawley rats were exposed to SHS for 5 weeks and then cortical tissues were collected. Nitroprotein enrichment was performed via 3-Nitro tyrosine (3-NT) immunoprecipitation of brain lysates proteins. Protein nitration was validated via Western blotting to confirm the presence of nitroproteins complemented by gel-free neuroproteomic analysis by data-dependent LC-MS/MS. We identified 29 differentially expressed proteins in the 3-NT-enriched samples; seven of these proteins were unique to SHS exposure. Network analysis revealed an association of the proteins to different cellular processes including oxidative stress, ROS generation, and cell death-related pathway. This confirms the association of oxidative stress mechanisms with SHS which may contribute to neuronal injury, an area that has not been well studied in the area smoking.

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Efeitos da administração de beta-bloqueador na remodelação ventricular induzida pelo tabagismo em ratos

Abstract: Administration of propranolol attenuated some of the variables of ventricular remodeling induced by the exposure to tobacco smoke in rats.

Cited by 7 publications

References 29 publications

Lipid damage is the best marker of oxidative injury during the cardiac remodeling process induced by tobacco smoke

Lipid damage is the best marker of oxidative injury during the cardiac remodeling process induced by tobacco smoke

Influência da taurina na remodelação cardíaca induzida pela exposição à fumaça do cigarro

Effect of Second-Hand Tobacco Smoke on the Nitration of Brain Proteins: A Systems Biology and Bioinformatics Approach

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