Endogenous free radical generating sources are involved in smoking-mediated dysfunction of nitric oxide biosynthesis in human coronary artery endothelial cells: An in vitro demonstration

Srivastava, Sudhesh; Barua, Rajat S.; Saha, Dhanonjoy C.; Eales-Reynolds, Lesley-Jane; DeVoe, Mary C.; Ambrose, John A.

doi:10.1016/s0735-1097(03)82432-4

Cited by 7 publications

(8 citation statements)

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“…Oxidative stress seems to play a fundamental role in nicotine’s mode of operation [14, 15]. Indeed, data of the present study strongly support this hypothesis since SOD, a scavenger for oxygen free radicals, significantly reduced CAM expression on cell surface.…”

Section: Discussionsupporting

confidence: 80%

“…In particular, oxygen free radicals [14, 15], mitogen-activated protein kinases (MAPKs) [29] and Src/Rb-Raf 1 pathways [30] have been studied. In the present study we confirmed the already documented role of MAPKs, since UO126, a specific inhibitor of extracellular signal-regulated kinases, reduced nicotine effects on CAM expression.…”

Section: Discussionmentioning

confidence: 99%

“…Positive control experiments included HCAECs stimulated with LPS (50 µg/ml) for 12 h. In additional control experiments, HCAECs were incubated with mecamylamine (500 µ M ), a nonselective nicotinic receptor inhibitor, or with α-bungarotoxin (500 µ M ), a specific nicotinic receptor inhibitor, 20 min before being stimulated with nicotine (10 –7 mol/l). As it has been suggested that promotion of oxidative stress might be a fundamental principle of nicotine’s mode of operation [14, 15], in another set of experiments, CAM expression was evaluated as above, but in cells preincubated for 30 min in the presence of the free radical scavenger superoxide dismutase (SOD; 500 U/ml). Lipid peroxidation is a well-established mechanism of cellular injury used as an indicator of oxidative stress in cells and tissues and measurement of malondialdehyde (MDA) has been used as an indicator of lipid peroxidation [16].…”

Section: Methodsmentioning

confidence: 99%

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HMG-CoA Reductase Inhibitors Reduce Nicotine-Induced Expression of Cellular Adhesion Molecules in Cultured Human Coronary Endothelial Cells

Cirillo¹,

Pacileo²,

Rosa³

et al. 2007

J Vasc Res

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Background: Smoking predisposes to the development of atherosclerosis and of its complications. The mechanisms responsible for these effects are not completely understood. We have investigated whether nicotine might promote a proatherosclerotic state in human coronary endothelial cells (HCAECs), studying the role of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors in preventing these phenomena. Methods and Results: Real-time PCR showed that nicotine induced a dose-dependent increase in mRNA levels for vascular cellular adhesion molecule-1 (VCAM-1)/intercellular adhesion molecule-1 (ICAM-1). Fluorescent-activated cell sorting analysis showed that nicotine induced expression of functionally active VCAM-1/ICAM-1, since they increased leukocyte adherence to HCAECs. Oxygen free radicals, Rho A and nuclear factor ĸB (NF-ĸB) play a pivotal role in modulating these effects. Indeed, nicotine caused oxygen free radical production as well as activation of Rho A and NF-ĸB pathways, evaluated by malondialdehyde levels, pulldown assay and by electrophoretic mobility shift assay, respectively. Superoxide dimutase, Rho A (Y-27639) and NF-ĸB inhibitors (pyrrolidine dithiocarbamate ammonium, Bay 11-7082) suppressed nicotine effects on CAM expression. HMG-CoA reductase inhibitors prevented these nicotine-mediated effects by inhibiting free radical generation and by modulating activation of Rho A and NF-ĸB pathways. Conclusions: Nicotine promotes CAM expression on HCAECs, shifting them toward a proatherosclerotic state. These effects might explain, at least in part, the deleterious cardiovascular consequences of cigarette smoking. HMG-CoA reductase inhibitors play an important role in preventing these phenomena.

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Section: Discussionsupporting

confidence: 80%

Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

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HMG-CoA Reductase Inhibitors Reduce Nicotine-Induced Expression of Cellular Adhesion Molecules in Cultured Human Coronary Endothelial Cells

Cirillo¹,

Pacileo²,

Rosa³

et al. 2007

J Vasc Res

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Section: How Is St Different From Smoking and Nrt?mentioning

confidence: 99%

“…Free oxidative radicals probably have the most important role in the development of endothelial injury and, subsequently, cardiovascular morbidity and mortality related to smoking [48,49]. These toxins are generated endogenously in response to burning, and they are effectively absorbed through the airway [48,49]. Other toxins that might be involved in the cardiovascular effects of smoking include 1,3-butadiene, polycyclic aromatic hydrocarbons, acetaldehyde, carbon monoxide, "tar," and carbon monoxide, all of which are produced by heat [50].…”

Section: How Is St Different From Smoking and Nrt?mentioning

confidence: 99%

How smokeless tobacco differs from smoking and nicotine replacement therapy

Arabi¹

2008

Curr Cardio Risk Rep

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Smokeless tobacco (ST) differs from smoking and nicotine replacement therapy (NRT) in its composition and cardiovascular side effects. Although ST and smoking have relatively similar effects on addiction, weight, blood pressure, and heart rate, ST has much milder effects on metabolic syndrome, myocardial infarction, stroke, and cardiovascular mortality. On the other hand, NRT has less effect on heart rate and blood pressure and helps to treat nicotine addiction and decrease the weight gain resulting from quitting tobacco products. NRT is considered safer than smoking and ST. The nicotine load from ST is higher than that from smoking, but the burning in smoking causes the release of many substances that are more cardiovascularly toxic than nicotine, which explains the prominent metabolic and cardiovascular effects of smoking. Nicotine seems to have only a secondary role in the cardiovascular effects of smoking.

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The pathophysiology of cigarette smoking and cardiovascular disease

Ambrose¹,

Barua²

2004

Journal of the American College of Cardiology

1,987

1,411

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Cigarette smoking (CS) continues to be a major health hazard, and it contributes significantly to cardiovascular morbidity and mortality. Cigarette smoking impacts all phases of atherosclerosis from endothelial dysfunction to acute clinical events, the latter being largely thrombotic. Both active and passive (environmental) cigarette smoke exposure predispose to cardiovascular events. Whether there is a distinct direct dose-dependent correlation between cigarette smoke exposure and risk is debatable, as some recent experimental clinical studies have shown a non-linear relation to cigarette smoke exposure. The exact toxic components of cigarette smoke and the mechanisms involved in CS-related cardiovascular dysfunction are largely unknown, but CS increases inflammation, thrombosis, and oxidation of low-density lipoprotein cholesterol. Recent experimental and clinical data support the hypothesis that cigarette smoke exposure increases oxidative stress as a potential mechanism for initiating cardiovascular dysfunction.

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Endogenous free radical generating sources are involved in smoking-mediated dysfunction of nitric oxide biosynthesis in human coronary artery endothelial cells: An in vitro demonstration

Cited by 7 publications

References 0 publications

HMG-CoA Reductase Inhibitors Reduce Nicotine-Induced Expression of Cellular Adhesion Molecules in Cultured Human Coronary Endothelial Cells

HMG-CoA Reductase Inhibitors Reduce Nicotine-Induced Expression of Cellular Adhesion Molecules in Cultured Human Coronary Endothelial Cells

How smokeless tobacco differs from smoking and nicotine replacement therapy

The pathophysiology of cigarette smoking and cardiovascular disease

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