ArticleBMC pharmacology & toxicology2018
Lipid damage is the best marker of oxidative injury during the cardiac remodeling process induced by tobacco smoke.
Article in BMC pharmacology & toxicology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 10 citations in OpenAlex.
- Comparative Genotoxicity and Mutagenicity of Cigarette, Cigarillo, and Shisha Tobacco Products in Epithelial and Cardiac Cells.Toxicological sciences : an official journal of the Society of Toxicology · 2021Article
- The role of glucose metabolism and insulin resistance in cardiac remodelling induced by cigarette smoke exposure.Journal of cellular and molecular medicine · 2021Article
- Lycopene Ameliorates Liver Inflammation and Redox Status in Mice Exposed to Long-Term Cigarette Smoke.BioMed research international · 2021Article
- Associations between Lifestyle Factors and Vitamin E Metabolites in the General Population.Antioxidants (Basel, Switzerland) · 2020Article
- Cinnamon-flavored electronic cigarette liquids and aerosols induce oxidative stress in human osteoblast-like MG-63 cells.Toxicology reports · 2020Article
- Protective Effects ofIn vivo (Athens, Greece)Article
Corrections and comments
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Authors and funding
14 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
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 μm
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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