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

Maria Angélica Martins Lourenço,Elisa Moya Kazmarek,Silmeia Garcia Zanati,Marcos Ferreira Minicucci,Mariana Gobbo Braz,Tatiana Fernanda Bachiega,Fábio Henrique Fernandes,Bruna Letícia Buzati Pereira,Sergio Alberto Rupp De Paiva,Leonardo Antonio Mamede Zornoff,Bertha Furlan Polegato,Ana Angélica Henrique Fernandes,Aline Garcia Aun,Paula Schmidt Azevedo

doi:10.1186/s40360-018-0268-4

Maria Angélica Martins Lourenço, Elisa Moya Kazmarek + Show 12 more

Open Access

https://doi.org/10.1186/s40360-018-0268-4

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Abstract

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.

Highlights

Oxidative stress is one potential mechanism that explain the direct effects of smoking on cardiac remodeling process
Since others have shown that 2 months of end of the article smoke (ETS) exposure is associated with change in ventricular function and structure, the aim of the study was to determine the cardiac levels of lipid hydroperoxide, protein carbonyl concentration and DNA damage in rats exposed to tobacco smoke
The rats were divided into 2 groups: group C composed by animals not exposed to cigarette smoke; group ETS composed by animals exposed to cigarette smoke

Summary

Introduction

Oxidative stress is one potential mechanism that explain the direct effects of smoking on cardiac remodeling process. No study has compared different myocardial products of macromolecule oxidation after tobacco smoke exposure. 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. In addition to the well-known effects of cigarette smoke on vascular systems, the direct effects of smoking on cardiac remodeling have been studied [2,3,4,5,6,7]. Oxidative stress occurs when there is an imbalance between reactive oxygen species (ROS) production and antioxidant systems. Tobacco smoke has more than 4000 chemical compounds and 1015 to 1017 free radicals that cause tissue inflammation and ROS production [14].

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