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      Cigarette smoking, endothelial injury and cardiovascular disease

      International Journal of Experimental Pathology

      Wiley

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          Free-radical chemistry of cigarette smoke and its toxicological implications.

           D Church,  W A Pryor (1985)
          Cigarette smoke contains two very different populations of free radicals, one in the tar and one in the gas phase. The tar phase contains several relatively stable free radicals; we have identified the principal radical as a quinone/hydroquinone (Q/QH2) complex held in the tarry matrix. We suggest that this Q/QH2 polymer is an active redox system that is capable of reducing molecular oxygen to produce superoxide, eventually leading to hydrogen peroxide and hydroxyl radicals. In addition, we have shown that the principal radical in tar reacts with DNA in vitro, possibly by covalent binding. The gas phase of cigarette smoke contains small oxygen- and carbon-centered radicals that are much more reactive than are the tar-phase radicals. These gas-phase radicals do not arise in the flame, but rather are produced in a steady state by the oxidation of NO to NO2, which then reacts with reactive species in smoke such as isoprene. We suggest that these radicals and the metastable products derived from these radical reactions may be responsible for the inactivation of alpha 1-proteinase inhibitor by fresh smoke. Cigarette smoke oxidizes thiols to disulfides; we suggest the active oxidants are NO and NO2. The effects of smoke on lipid peroxidation are complex, and this is discussed. We also discuss the toxicological implications for the radicals in smoke in terms of a number of radical-mediated disease processes, including emphysema and cancer.
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            Cigarette smoking is associated with dose-related and potentially reversible impairment of endothelium-dependent dilation in healthy young adults.

            Cigarette smoking is the most important modifiable risk factor for atherosclerosis. Endothelial dysfunction is an early event in atherogenesis, and we hypothesized that smoking might be associated with endothelial damage in the systemic arteries of otherwise healthy young adults. We studied noninvasively the brachial arteries of 200 subjects aged 15 to 57 years, all normotensive, nondiabetic with cholesterol level < or = 240 mg/dL and no family history of premature vascular disease: 80 control subjects aged 16 to 56 years (mean, 35), 80 current smokers aged 15 to 55 years (mean, 33), and 40 former smokers aged 25 to 57 years (mean, 38). Total lifetime amount smoked varied from 1 to 75 pack years in the smokers. Using high-resolution ultrasound, vessel diameter was measured at rest, during reactive hyperemia (with flow increase causing endothelium-dependent dilation), and after sublingual glyceryl trinitrate (GTN, an endothelium-independent vasodilator). Flow-mediated dilation (FMD) was observed in all the control subjects (10 +/- 3.3%; range, 4% to 22%) but was impaired or absent in the smokers (4 +/- 3.9%; range, 0% to 17%; P < .0001). FMD in the smokers was inversely related to lifetime dose smoked (6.6 +/- 4.0% in very light smokers, 4.0 +/- 3.1% in light smokers, 3.2 +/- 3.2% in moderate smokers, and 2.6 +/- 1.2% in heavy smokers; P < .01). FMD for the former smokers was 5.1 +/- 4.1% (range, 0% to 15%). In a multivariate model adjusting for age, sex, cholesterol, smoking history, and vessel size, former smoking was associated with a higher FMD than current smoking (P = .07); when only male former and current smokers were considered, the higher FMD was significant (P = .0001) but not for female smokers (P = .24). GTN caused dilation in all subjects (control subjects, 20 +/- 5.2%; smokers, 17 +/- 5.8%; former smokers, 17.4 +/- 5.4%). Vessel diameter, baseline flow, and degree of reactive hyperemia (Doppler estimated) were similar in all groups. Cigarette smoking is associated with dose-related and potentially reversible impairment of endothelium-dependent arterial dilation in asymptomatic young adults, consistent with endothelial dysfunction.
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              Acute and chronic effects of cigarette smoking on exhaled nitric oxide.

              Cigarette smoking is associated with an increased risk of respiratory tract infections, chronic airway disease, and cardiovascular diseases, all of which may be modulated by endogenous nitric oxide (NO). We have investigated whether cigarette smoking reduces the production of endogenous NO. We compared exhalations of 41 current cigarette smokers with normal lung function and 73 age-matched non-smoking controls. Peak exhaled NO levels were measured by a modified chemiluminescence analyzer. The effects of inhaling a single cigarette in smokers were also measured. In control subjects we also measured the effects of inhalation of NO itself and carbon monoxide, both constituents of tobacco smoke. Peak exhaled NO concentrations were significantly reduced in smokers (42 +/- 3.9 compared with 88 +/- 2.7 parts per billion in nonsmokers, p < 0.01), with a significant relation between the exhaled NO and cigarette consumption (r = 0.77, p < 0.001). Smoking a single cigarette also significantly (p < 0.02), but transiently, reduced exhaled NO. Inhalation of carbon monoxide and NO had no effect on exhaled NO in normal subjects. Cigarette smoking decreased exhaled NO, suggesting that it may inhibit the enzyme NO synthase. Since endogenous NO is important in defending the respiratory tract against infection, in counteracting bronchoconstriction and vasoconstriction, and in inhibiting platelet aggregation, this effect may contribute to the increased risks of chronic respiratory and cardiovascular disease in cigarette smokers.
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                Author and article information

                Journal
                10.1046/j.1365-2613.2000.00162.x
                10971743
                2517732

                http://doi.wiley.com/10.1002/tdm_license_1.1

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