Tobacco Smoke Induces Ventricular Remodeling Associated with an Increase in NADPH Oxidase Activity

Abstract

Background: Recent studies have assessed the direct effects of smoking on cardiac remodeling and function. However, the mechanisms of these alterations remain unknown. The aim of this study was to investigate de role of cardiac NADPH oxidase and antioxidant enzyme system on ventricular remodeling induced by tobacco smoke. Methods: Male Wistar rats that weighed 200-230 g were divided into a control group (C) and an experimental group that was exposed to tobacco smoke for a period of two months (ETS). After the two-month exposure period, morphological, biochemical and functional analyses were performed. Results: The myocyte cross-sectional area and left ventricle end-diastolic dimension was increased 16.2% and 33.7%, respectively, in the ETS group. The interstitial collagen volume fraction was also higher in ETS group compared to the controls. In addition to these morphological changes, the ejection fraction and fractional shortening were decreased in the ETS group. Importantly, these alterations were related to augmented heart oxidative stress, which was characterized by an increase in NADPH oxidase activity, increased levels of lipid hydroperoxide and depletion of antioxidant enzymes (e.g., catalase, superoxide dismutase and glutathione peroxidase). In addition, cardiac levels of IFN-γ, TNF-α and IL-10 were not different between the groups. Conclusion: Cardiac alterations that are induced by smoking are associated with increased NADPH oxidase activity, suggesting that this pathway plays a role in the ventricular remodeling induced by exposure to tobacco smoke.

Resveratrol attenuates oxidative stress during experimental periodontitis in rats exposed to cigarette smoke inhalation

“…It is known that NOx and nitrotyrosine (residues of protein nitrosylated by ROS formed by the combination of nitric oxide and superoxide) are increased significantly in periodontal tissue during EP . In vitro and in vivo studies have also demonstrated that NOX production and activation can be induced by CSI; findings that have also been shown in human studies . In this regard, a recent study demonstrated reduced activation of NADPH oxidase/ROS/NF‐κB pathways in human fibroblast‐like synoviocytes after resveratrol treatment, leading to the suppression of particulate matter air pollution‐induced COX‐2 expression and PGE2 release .…”

The −930A>G polymorphism of the CYBA gene is associated with premature coronary artery disease. A case–control study and gene–risk factors interactions

“…Short exposure of human and animal endothelial cells to cigarette smoke extracts resulted in a large increase in O 2 − production, which was inhibited by several NOX inhibitors [25]. An increased NADPH oxidase activity was observed among others in the ventricular remodeling induced by tobacco smoke exposure [26]. The −930A>G CYBA polymorphism was also analyzed in the context of an association between cigarette smoking and carotid intima-media thickness (IMT), a marker of subclinical atherosclerosis [27].…”

Aldosterone is not Involved in the Ventricular Remodeling Process Induced by Tobacco Smoke Exposure

“…Interestingly, tobacco smoke did not increase myocardial inflammatory cytokines in our study. Although we have already observed these cytokine patterns in previous studies, ICAM-1 expression has not yet been evaluated in tobacco exposure models [8,11]. Importantly, the expression of adhesion molecules is essential for the influx of inflammatory cells into the myocardium.…”

“…The mechanisms involved in this remodeling process are not completely known. Potential mechanisms for these alterations include inflammation [8,11], oxidative stress [8,11], metalloproteinase [5] and mitogen-activated protein kinase activation [6], and hemodynamic and neurohormonal changes, such as renin-angiotensinaldosterone system (RAAS) activation [12].…”