Urinary excretion of three nucleic acid oxidation adducts and isoprostane F2α measured by liquid chromatography-mass spectrometry in smokers, ex-smokers, and nonsmokers

Harman, S. Mitchell; Liang, Lynn; Tsitouras, Panayiotis D.; Gucciardo, Frank; Heward, Christopher B.; Reaven, Peter D.; Wei, Ping; Ahmed, Alaa Elsafi; Cutler, Richard G.

doi:10.1016/j.freeradbiomed.2003.07.003

Cited by 80 publications

(58 citation statements)

References 44 publications

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“…The mean level of all isoprostanes analyzed (iPF 2a -III, 2,3-dinor-iPF 2a -III, 15-epi-iPF 2a -III, 8,12-iso-iPF 2a -VI, and iPF 2a -VI) was significantly higher in women than in men in units of pg/mg creatinine but not in units of mg/day. The same difference was observed in both smokers and nonsmokers, and these results are consistent with iPF 2a -III and 2,3-dinor-iPF 2a -III values (pg/mg creatinine) reported in the literature (55,67). iPF 2a -III in plasma was also reported to be significantly higher in women than in men (24).…”

Section: Results For Human Urinesupporting

confidence: 91%

“…iPF 2a -III in plasma was also reported to be significantly higher in women than in men (24). The reason for the higher level of isoprostanes in women was not clear, although greater susceptibility to lipid oxidation in female smokers is a possibility (55). Interestingly, in our study, the total excretion per day of analytes was not different by gender.…”

Section: Results For Human Urinecontrasting

confidence: 48%

“…The method showed potential for the routine determination of urinary iPF 2a -III and 2,3-dinor-iPF 2a -III in clinical samples. Several applications of iPF 2a -III quantitation by LC-MS were reported to evaluate the role of oxidative stress in different diseases (31,32,(55)(56)(57). Recently, F 2 -isoprostane regioisomers and diastereomers formed in vitro were separated and identified by LC-MS (58).…”

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confidence: 99%

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

Yan

Byrd

Ogden

2007

Journal of Lipid Research

105

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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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Section: Results For Human Urinesupporting

confidence: 91%

Section: Results For Human Urinecontrasting

confidence: 48%

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confidence: 99%

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

Yan

Byrd

Ogden

2007

Journal of Lipid Research

105

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“…F 2 -isoprostane forms through lipid peroxidation reactions with hydroxyl radicals, the same radicals that form 8-hydroxydeoxyguanosine (8-OhdG) adducts when reacted with DNA. Furthermore, recent work shows that urinary levels of F 2 -isoprostane and 8-OhdG are correlated (7). Two noncontrolled exercise intervention studies in men have noted decreases in oxidative stress as measured by F 2 -isoprostanes (8,9).…”

Section: Introductionmentioning

confidence: 99%

Exercise Effect on Oxidative Stress Is Independent of Change in Estrogen Metabolism

Schmitz

Warren

Rundle

et al. 2008

Cancer Epidemiology, Biomarkers &Amp; Prevention

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Purpose: The effect of exercise training on lipid peroxidation and endogenous estrogens is not well understood in premenopausal women. Exercise effects on these variables could mediate observed associations of exercise with hormonally related cancers, including breast cancer. The purpose of the study is to determine the effect of 15 weeks of aerobic exercise on lipid peroxidation, endogenous estrogens, and body composition in young, healthy eumenorrheic women. Methods: Fifteen sedentary premenopausal women (18-25 years) participated. Pre-and post-exercise training urine collection (three 24-h samples) started 48 h after most recent exercise session for analysis of a marker of lipid peroxidation (F 2 -isoprostane) and endogenous estrogens, including 2-hydroxyestrogens, 4-hydroxyestrogens, 16-A-hydroxyestrone, and ratios of these metabolites (2:16, 2:4). Body composition was measured by dual-energy X-ray absorptiometry, and F 2 -isoprostanes and estrogens were measured by gas chromatography-mass spectrometry. Results: Aerobic exercise resulted in a 34% decrease in F 2 -isoprostane (P = 0.02), a 10% increase in fitness (P = 0.004), a 1.2 kg decrease in body mass (P = 0.007), and a 1.8 kg decrease in fat mass (P = 0.04). No significant changes were noted in estrogens.

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“…Exposure to tobacco smoke increases inflammation, oxidative stress [1][2][3][4][5][6][7][8][9][10] and decreases antioxidant expression. [11][12][13][14][15] Direct and indirect studies have demonstrated that oxidative stress from reactive oxygen species (ROS) generated through mitochondria, xanthine oxidase, and the NADPH oxidase system [16][17][18][19][20][21] is one of the important factors in the pathogenesis of myocardial ischemia. Decreased infarct size in superoxide dismutase (SOD)-producing transgenic mice suggests direct evidence for the role of involvement of ROS in MI.…”

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confidence: 99%

Antioxidant N-acetyl cysteine reverses cigarette smoke-induced myocardial infarction by inhibiting inflammation and oxidative stress in a rat model

Khanna

Mehra

2012

Laboratory Investigation

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The contribution of chronic tobacco exposure in determining post-myocardial infarction (MI) left ventricular (LV) remodeling and possible therapeutic strategies has not been investigated systematically. In this small animal investigation, we demonstrate that chronic tobacco smoke exposure leading up to acute MI in rats is associated with greater histological extent of myocardial necrosis and consequent worse LV function. These findings are associated with increased transcriptomic expression of pro-inflammatory cytokines, tissue repair molecules and markers of oxidative stress in the myocardium. The results demonstrate that an N-acetyl cysteine (NAC) treatment significantly reduced tobacco-exposed induced infarct size and percent fractional shortening. A significantly increased LV end-systolic diameter was observed in tobacco-exposed sham compared to tobacco-naïve sham (4.92 ± 0.41 vs 3.45 ± 0.33; Po0.05), and tobacco-exposed MI compared to tobacco-naïve MI (8.24±0.3 vs 6.1±0.49; Po0.01) rats. Decreased intracardiac mRNA expression of the markers of inflammation, tissue repair and oxidative stress and circulating levels of pro-inflammatory cytokines accompanied these positive effects of NAC. The treatment of tobacco-exposed MI rats with NAC resulted in significantly increased levels of intracardiac mRNA expression of antioxidants, including superoxide dismutase, thioredoxin and nuclear factor-E2-related factor 2, as well as circulating levels of glutathione (7 ± 0.12 vs 10 ± 0.18; Pp0.001), where the levels were almost identical to the tobacco-naïve sham rats. These findings identify a novel post-infarction therapy for amelioration of the adverse effects of tobacco exposure on the infracted myocardium and advocate the use of dietary supplement antioxidants for habitual smokers to prevent and reverse cardiovascular adverse effects in the absence of successful achievement of cessation of smoking. Globally, tobacco smoke exposure remains a significant risk for the development of acute myocardial infarction (MI) irrespective of ethic or gender disparities. Exposure to tobacco smoke increases inflammation, oxidative stress 1-10 and decreases antioxidant expression. [11][12][13][14][15] Direct and indirect studies have demonstrated that oxidative stress from reactive oxygen species (ROS) generated through mitochondria, xanthine oxidase, and the NADPH oxidase system 16-21 is one of the important factors in the pathogenesis of myocardial ischemia. Decreased infarct size in superoxide dismutase (SOD)-producing transgenic mice suggests direct evidence for the role of involvement of ROS in MI. 22,23 In limited investigations, the use of antioxidants such as mercaptopropionyl glycine, edaravone and probucol have demonstrated varied effects on remodeling in animal models of MI, [24][25][26][27][28][29][30][31][32] with improvement in collagen content and histological changes. In this study, we sought to delineate the role of chronic tobacco smoke leading up to an acute MI by focusing on oxidative stress coupled with inflammat...

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Urinary excretion of three nucleic acid oxidation adducts and isoprostane F2α measured by liquid chromatography-mass spectrometry in smokers, ex-smokers, and nonsmokers

Cited by 80 publications

References 44 publications

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

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

Exercise Effect on Oxidative Stress Is Independent of Change in Estrogen Metabolism

Antioxidant N-acetyl cysteine reverses cigarette smoke-induced myocardial infarction by inhibiting inflammation and oxidative stress in a rat model

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