Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2018 Nov 16;19(1):74.
doi: 10.1186/s40360-018-0268-4.

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

Affiliations

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

Maria Angélica Martins Lourenço et al. BMC Pharmacol Toxicol. .

Abstract

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.

Keywords: Cigarette smoke; Comet assay; DNA damage; Protein carbonyl groups.

PubMed Disclaimer

Conflict of interest statement

Ethics approval

All experiments and procedures were performed in accordance with the National Institute of Health Guide for the Care and Use of Laboratory Animals and were approved by the Animal Ethics Committee of Botucatu Medical School.

Consent for publication

Not applicable.

Competing interests

The authors declare that they have no competing interests.

Publisher’s Note

Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

Figures

Fig. 1
Fig. 1
Myocyte cross-sectional area (CSA) a. C group. b Exposed to Tobacco Smoke group. CSA was higher in ETS group compared to C group
Fig. 2
Fig. 2
Comet assay. a Tail intensity in cardiac tissue from the C group. b Tail intensity in cardiac tissue from the ETS group. c Tail intensity in blood from the c group d. Tail intensity in blood from the ETS group. There were no differences between groups in the mean tail intensity in the blood or in the cardiac tissue

Similar articles

Cited by

References

    1. Jamal A, King BA, Neff LJ, Whitmill J, Babb SD, Graffunder CM. Current cigarette smoking among adults - United States, 2005-2015. MMWR Morb Mortal Wkly Rep. 2016;65:1205–1211. doi: 10.15585/mmwr.mm6544a2. - DOI - PubMed
    1. Castardeli E, Paiva SA, Matsubara BB, Matsubara LS, Minicucci MF, Azevedo PS, et al. Chronic cigarette smoke exposure results in cardiac remodeling and impaired ventricular function in rats. Arq Bras Cardiol. 2005;84:320–324. doi: 10.1590/S0066-782X2005000400009. - DOI - PubMed
    1. Castardeli E, Duarte DR, Minicucci MF, Azevedo PS, Matsubara BB, Matsubara LS, et al. Tobacco smoke-induced left ventricular remodelling is not associated with metalloproteinase-2 or −9 activation. Eur J Heart Fail. 2007;9:1081–1085. doi: 10.1016/j.ejheart.2007.09.004. - DOI - PubMed
    1. Zornoff LA, Matsubara LS, Matsubara BB, Okoshi MP, Okoshi K, Dal Pai-Silva M, et al. Beta-carotene supplementation attenuates cardiac remodeling induced by one-month tobacco-smoke exposure in rats. Toxicol Sci. 2006;90:259–266. doi: 10.1093/toxsci/kfj080. - DOI - PubMed
    1. Rafacho BP, Azevedo PS, Polegato BF, Fernandes AA, Bertoline MA, Fernandes DC, et al. Tobacco smoke induces ventricular remodeling associated with an increase in NADPH oxidase activity. Cell Physiol Biochem. 2011;27:305–312. doi: 10.1159/000327957. - DOI - PubMed

Publication types

LinkOut - more resources