Molecular and Biochemical Changes of the Cardiovascular System due to Smoking Exposure

Abstract

Cigarette smoking (CS) is a major health hazard particularly for the cardiovascular system and cancer. The mechanisms involved in CS-related cardiovascular dysfunction have been largely debated. CS increases inflammation, thrombosis, and oxidation of low-density lipoproteins. Recent experimental and clinical data support the hypothesis that cigarette smoke exposure increases oxidative stress as a potential mechanism for initiating cardiovascular dysfunction. Cardiac myocytes, as well as and other long-lived postmitotic cells show dramatic smoke-related alterations that mainly affect the mitochondria and lysosomal compartment. Mitochondria are primary sites of reactive oxygen species formation that cause progressive damage to mitochondrial DNA and proteins in parallel to intralysosomal lipofuscin accumulation. There is amassing evidence that various mechanisms may contribute to accumulation of damaged mitochondria following initial oxidative injury. Such mechanisms may include clonal expansion of defective mitochondria, decreased propensity of altered mitochondria to become autophagocytosed, suppressed autophagy because of heavy lipofuscin loading of lysosomes and decreased efficiency of specific proteases involved into mitochondrial degradation. A possible interplay between microtubule plasticity and oxidative stress also exists in cardiomyocytes, so this could represent another potential mechanism by which smoking induces/accelerates atherosclerosis.

Cerium Oxide Nanoparticles Inhibits Oxidative Stress and Nuclear Factor-κB Activation in H9c2 Cardiomyocytes Exposed to Cigarette Smoke Extract

“…Cigarette smoke has been identified as a major risk factor for cardiovascular diseases, and increased oxidative stress and inflammation are considered to be an important mechanism of cardiovascular remodeling induced by smoking (Leone et al, 2008;Armani et al, 2009;Csiszar et al, 2009;Minicucci et al, 2009). Recent studies in rodent models of smoking have shown that acute CS exposure causes increased cardiac oxidative stress that is associated with depleted cellular antioxidant capacity (Bernhard and Wang, 2007;Ramesh et al, 2008).…”

“…It is becoming increasingly evident that cigarette smoke exacerbates endothelium injury and the development of atherosclerosis. Several recent studies also demonstrated that chronic cigarette exposure can result in cardiomyopathy, characterized by the progressive and irreversible deterioration of cardiac function associated with interstitial fibrosis, cardiac myocyte vacuolization, arteriolar hyalinosis, and immune reaction in the heart (Hartz et al, 1984;Leone et al, 2008;Armani et al, 2009;Minicucci et al, 2009). Although our understanding of the pathogenesis of smoke cardiomyopathy is still limited, several lines of evidence suggest that both oxidative stress and inflammatory responses play an essential role in the biological processes induced by smoke (Ambrose and Barua, 2004;Csiszar et al, 2009).…”

Smoking Status is Associated with Serum High Molecular Adiponectin Levels in Community-Dwelling Japanese Men

“…Smoking has been known to be associated with increased oxidative stress and nicotine. Oxidative stress can damage many cell components and functions, including DNA, mitochondrial metabolism, lipid, and protein 24,25) . Iwashima et al 8) demonstrated that H2O2 and nicotine generated by smoking reduced mRNA expression and secretion of adiponectin in a dosedependent manner in cultured mouse 3T3-L1 adipocytes.…”

6-Gingerol Attenuates Hydrogen Peroxide-induced DNA Damage in Human Umbilical Vein Endothelia Cells

“…The most important function of GSH is to protect against oxidative damage caused by ROS through enzymatic and nonenzymatic reactions (Meister 1994). In many diseases, including atherosclerosis, cancer, neurodegenerative disease, and aging, GSH can scavenge of free radicals, modulate hydrogen peroxide level and interact with nitric oxide pathways (Armani et al, 2009). There is evidence that 6-gingerol pretreatment significantly enhanced the levels of reduced GSH and activities of superoxide dismutase and catalase against cisplatin-induced oxidative stress and renal dysfunction (Kuhad et al, 2006).…”