Quitting Cigarette Smoking Results in a Fast Improvement of in vivo Oxidation Injury (Determined via Plasma, Serum and Urinary Isoprostane)

Pilz, Heidemarie; Oguogho, A.; Chehne, F.; Lupattelli, Graziana; Palumbo, Barbara; Sinzinger, H.

doi:10.1016/s0049-3848(00)00249-8

Cited by 72 publications

(41 citation statements)

References 19 publications

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“…Quitting smoking led to decreased 15-F 2t -IsoP levels (46,48); restarting smoking resulted in increased levels (49). 8-oxodG levels were also elevated in smokers (30,43,50,51).…”

Section: Discussionmentioning

confidence: 99%

Relationship between Urinary 15-F2t-Isoprostane and 8-Oxodeoxyguanosine Levels and Breast Cancer Risk

Rössner

Gammon

Terry

et al. 2006

Cancer Epidemiology, Biomarkers &Amp; Prevention

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To evaluate the role of oxidative stress in breast cancer, we measured urinary levels of 15-F 2t -isoprostane (15-F 2t -IsoP) and 8-oxodeoxyguanosine (8-oxodG) in 400 cases and 401 controls, participants of the Long Island Breast Cancer Study Project. We also analyzed the effect of different factors that are associated with oxidative stress and might influence 15-F 2t -IsoP and 8-oxodG levels. We observed a statistically significant trend in breast cancer risk with increasing quartiles of 15-F 2t -IsoP levels [odds ratio (OR), 1.25; 95% confidence interval (95% CI), 0.81-1.94; OR, 1.53; 95% CI, 0.99-2.35; OR, 1.88; 95% CI, 1.23-2.88, for the 2nd, 3rd, and 4th quartile relative to the lowest quartile, respectively; P trend = 0.002]. Although it is possible that increased levels may reflect the stress associated with recent treatment, the positive association was also observed when the analyses were restricted to case women for whom chemotherapy and radiation therapy had not yet been initiated at the time of the urine collection. The association with the highest quartile compared with lowest quartile of 15-F 2t -IsoP was similar across strata of age, physical activity, fruit and vegetable intake, alcohol intake, cigarette smoking, body mass index, and menopausal status. We did not observe any association of breast cancer risk with 8-oxodG levels, but when cases with radiation treatment were removed from the analysis, a significant inverse trend (P = 0.04) was observed. Among controls, levels of 15-F 2t -IsoP were higher among current cigarette smokers but did not differ by the amount of physical activity, fruit and vegetable intake, alcohol intake, body mass index, and menopausal status. Among controls, levels of 8-oxodG were higher among postmenopausal women and current and former cigarette smokers but did not differ by the other factors. In summary, our results suggest that urinary markers of lipid peroxidation and oxidative DNA damage may be associated with breast cancer risk. (Cancer Epidemiol Biomarkers Prev 2006;15(4):639 -44)

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“…Quitting smoking led to decreased 15-F 2t -IsoP levels (46,48); restarting smoking resulted in increased levels (49). 8-oxodG levels were also elevated in smokers (30,43,50,51).…”

Section: Discussionmentioning

confidence: 99%

Relationship between Urinary 15-F2t-Isoprostane and 8-Oxodeoxyguanosine Levels and Breast Cancer Risk

Rössner

Gammon

Terry

et al. 2006

Cancer Epidemiology, Biomarkers &Amp; Prevention

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“…Later, Yamaguchi et al 23 suggested that peroxynitrite (generated by a reaction between NO and superoxide anion) is involved in the oxidative modification of LDL in smokers' blood. Further support for these findings comes from studies by Pilz et al, 24 Reilly et al, 25 and Solak et al, 26 showing increased lipid oxidation, signs of oxidative stress, and impairment of antioxidant systems. It is well known that only oxidatively modified LDLs are recognized by macrophage scavenger receptors, taken up by these macrophages and causing their transformation into foam cells, which are essential elements in lipid deposition and plaque formation.…”

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confidence: 86%

Smoking and Cardiovascular Disease

Meßner

Bernhard

2014

ATVB

762

275

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Abstract-Smoking represents one of the most important preventable risk factors for the development of atherosclerosis. The present review aims at providing a comprehensive summary of published data from clinical and animal studies, as well as results of basic research on the proatherogenic effect of smoking. Extensive search and review of literature revealed a vast amount of data on the influence of cigarette smoke and its constituents on early atherogenesis, particularly on endothelial cells. Vascular dysfunction induced by smoking is initiated by reduced nitric oxide (NO) bioavailability and further by the increased expression of adhesion molecules and subsequent endothelial dysfunction. Smoking-induced increased adherence of platelets and macrophages provokes the development of a procoagulant and inflammatory environment. After transendothelial migration and activation, macrophages take up oxidized lipoproteins arising from oxidative modifications and transdifferentiate into foam cells. In addition to direct physical damage to endothelial cells, smoking induces tissue remodeling, and prothrombotic processes together with activation of systemic inflammatory signals, all of which contribute to atherogenic vessel wall changes. There are still great gaps in our knowledge about the effects of smoking on cardiovascular disease. However, we know that smoking cessation is the most effective measure for reversing damage that has already occurred and preventing fatal cardiovascular outcomes. Clinical DataEvidence for smoking-induced initial vascular damage and endothelial dysfunction stems from an array of clinical studies analyzing endothelial function using various techniques. 6 As mentioned above, in 1993, Celermajer et al 5 were able to show that continuous smoking impairs FMD of the brachial artery in a dose-dependent manner, shown by the strong association between FMD and pack years smoked. This was also found to be the case with coronary arteries in a study by Zeiher et al. 7 Interestingly, reduction of endothelium-dependent dilatation by smoking was reversible, and significant improvement of FMD 1 year after cessation has been reported. 8 Likewise, a recent study of Amato et al 9 revealed that smoking light cigarettes impairs FMD as much as smoking regular cigarettes, arguing against light cigarettes as a less harmful alternative.Measurement of FMD represents a useful tool to assess the effects of smoking on the vascular wall. Independent of its FMD reducing activity, smoking was shown to induce other proatherogenic alterations in the vascular wall (eg, by deposition of smoke chemicals). The time needed to restore interrupted functions of the vascular endothelium will depend on the specific process that has caused the endothelial damage; some alterations of the endothelial wall may vanish more rapidly than others, without these being reflected by improved FMD.Clinical studies assessing the interrelation of secondhand smoking and FMD reported strong correlations. Secondhand smoking was shown to impair endo...

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“…Vitamin C supplementation decreased iPF 2a -III in plasma from smokers (23) and nonsmokers exposed to environmental tobacco smoke (24). Plasma, serum, and urinary levels of iPF 2a -III decreased significantly after quitting cigarette smoking (25,26) and increased after restarting smoking (27).…”

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confidence: 99%

Quantitation of isoprostane isomers in human urine from smokers and nonsmokers by LC-MS/MS

Yan

Byrd

Ogden

2007

Journal of Lipid Research

103

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A simple, rapid liquid chromatography-tandem mass spectrometry method was developed to identify and quantitate in human urine the isoprostanes iPF 2a -III, 15-epiiPF 2a -III, iPF 2a -VI, and 8,12-iso-iPF 2a -VI along with the prostaglandin PGF 2a and 2,3-dinor-iPF 2a -III, a metabolite of iPF 2a -III. Assay specificity, linearity, precision, and accuracy met the required criteria for most analytes. The urine sample storage stability and standard solution stability were also tested.The methodology was applied to analyze 24 h urine samples collected from smokers and nonsmokers on controlled diets. The results for iPF 2a -III obtained by our method were significantly correlated with results by an ELISA, although an ?2-fold high bias was observed for the ELISA data. For iPF 2a -III and its metabolite 2,3-dinoriPF 2a -III, smokers had significantly higher concentrations than nonsmokers (513 6 275 vs. 294 6 104 pg/mg creatinine; 3,030 6 1,546 vs. 2,046 6 836 pg/mg creatinine, respectively). The concentration of iPF 2a -VI tended to be higher in smokers than in nonsmokers; however, the increase was not statistically significant in this sample set. Concentrations of the other three isoprostane isomers showed no trends toward differences between smokers and nonsmokers. Among smokers, the daily output of two type VI isoprostanes showed a weak correlation with the amount of tobacco smoke exposure, as determined by urinary excretion of total nicotine equivalents.-Yan, W., G. D. Byrd, and M. W. Ogden. Quantitation of isoprostane isomers in human urine from smokers and nonsmokers by LC-MS/MS.

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Quitting Cigarette Smoking Results in a Fast Improvement of in vivo Oxidation Injury (Determined via Plasma, Serum and Urinary Isoprostane)

Cited by 72 publications

References 19 publications

Relationship between Urinary 15-F2t-Isoprostane and 8-Oxodeoxyguanosine Levels and Breast Cancer Risk

Relationship between Urinary 15-F2t-Isoprostane and 8-Oxodeoxyguanosine Levels and Breast Cancer Risk

Smoking and Cardiovascular Disease

Quantitation of isoprostane isomers in human urine from smokers and nonsmokers by LC-MS/MS

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