脂质损伤是烟草烟雾诱导的心脏重塑过程中氧化损伤的最佳标志物。
Lipid damage is the best marker of oxidative injury during the cardiac remodeling process induced by tobacco smoke.
作者信息
Lourenço Maria Angélica Martins, Braz Mariana Gobbo, Aun Aline Garcia, Pereira Bruna Letícia Buzati, Fernandes Fábio Henrique, Kazmarek Elisa Moya, Bachiega Tatiana Fernanda, Zanati Silmeia Garcia, Azevedo Paula Schmidt, Polegato Bertha Furlan, Fernandes Ana Angélica Henrique, de Paiva Sergio Alberto Rupp, Zornoff Leonardo Antonio Mamede, Minicucci Marcos Ferreira
机构信息
Internal Medicine Department, Botucatu Medical School, UNESP - São Paulo State University, Botucatu, Brazil.
Department of Anesthesiology, Botucatu Medical School, UNESP - São Paulo State University, Botucatu, Brazil.
出版信息
BMC Pharmacol Toxicol. 2018 Nov 16;19(1):74. doi: 10.1186/s40360-018-0268-4.
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 μm and ETS = 347.5 ± 15.1 μm, 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.
背景
氧化应激是解释吸烟对心脏重塑过程直接影响的一种潜在机制。然而，尚无研究比较烟草烟雾暴露后不同的心肌大分子氧化产物。因此，本研究的目的是调查暴露于烟草烟雾的大鼠心脏组织中的脂质过氧化氢（LH）水平、蛋白质羰基浓度和DNA损伤。
方法
将雄性Wistar大鼠分为两组：C组（对照组，n = 14），由未暴露于香烟烟雾的动物组成；ETS组（暴露于烟草烟雾组，n = 14），由暴露于香烟烟雾的动物组成。动物暴露于烟草烟雾2个月，并进行形态学、生化和功能分析。
结果
ETS组心脏可替宁水平升高。此外，ETS组心肌细胞横截面积更大。（C组 = 266.6 ± 23.2μm，ETS组 = 347.5 ± 15.1μm，p < 0.001）。ETS组心脏LH高于C组（C组 = 196.4 ± 51.5nmol/g，ETS组 = 331.9 ± 52.9nmol/g，p < 0.001）。然而，心脏蛋白质羰基浓度或DNA损伤在组间无差异。
结论
因此，我们的结果表明，在该模型中，脂质损伤是2个月烟草烟雾暴露诱导的心脏重塑过程中氧化损伤良好的标志物。
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