Plasma Fluorescent Oxidation Products as Potential Markers of Oxidative Stress for Epidemiologic Studies

Department of Nutrition, Harvard School of Public Health, Boston, MA 02115, USA.
American Journal of Epidemiology (Impact Factor: 5.23). 10/2007; 166(5):552-60. DOI: 10.1093/aje/kwm119
Source: PubMed


Currently lacking are stable and easily measured biomarkers that can reflect oxidative stress in humans. Fluorescent oxidation products may fulfill all three of these criteria. Fasting plasma levels of fluorescent oxidation products were measured in 286 controls in a study of coronary heart disease among US men aged 47-81 years; the study concluded in 2006. Other biomarkers in plasma were also measured, and cardiovascular risk factors such as smoking, hypertension, age, and physical activity were assessed by questionnaire. Indicators of oxidative stress, including smoking, hypertension, and reduced renal function, were associated with greater fluorescent oxidation products in both age- and multivariate-adjusted analyses (for each, p for trend < 0.01). In a multivariate-adjusted analysis, levels of fluorescent oxidation products were 45% higher in current smokers than in never smokers and 61% higher in men who smoked more than 25 cigarettes/day versus 1-4 cigarettes/day. The levels of this marker were 17% higher in hypertensive men than in normotensive men and 20% higher in men in the lowest versus the highest quartile of glomerular filtration rate. Levels were 57% higher in men with both hypertension and reduced renal function than in men with neither. The association of fluorescent oxidation products with several indicators of oxidative stress suggests that this measure could be a useful global marker of oxidative stress for large epidemiologic studies.

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    • "Plasma fluorescent oxidation has been found to be an independent marker for future risk of coronary heart disease in men apart from conventional risk factors like lipid parameters and Fig. 8. Representative photographs of ferrous chloride (FeCl 2 )-applied carotid arterial tissues stained with hematoxylin-eosin. inflammatory markers (Wu et al., 2007). In the present study, criton X-100 treatment increased FI compared to normal control animals. "
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    ABSTRACT: The increased mortality rate due to atherothrombotic events and related complications has necessitated the search for new pharmacological agents. Hyperlipidemia, thrombosis and oxidative stress are the primary underlying concerns in the pathogenesis of atherosclerosis. Metformin, although proved to be beneficial in micro and macrovascular complications of diabetes mellitus, its effects on pure cardiovascular subjects are still debatable. Hence, the aim of the present study was to investigate the effects of metformin on atherothrombotic risk factors in experimental hyperlipidemic rats. Hyperlipidemia was induced by an intra-peritoneal injection of criton X-100 (25 mg/kg). Assessment of the effects of metformin (300 mg/kg/day, 400 mg/kg/day and 500 mg/kg/day) on lipid profile, coagulation time (activated partial thromboplastin time and prothrombin time), fibrinogen level, thrombosis, lipid peroxidation, antioxidant enzymes level, plasma fluorescent oxidation products and aortic nitrite level revealed an overall improvement in the lipid profile at the dose of 400 mg/kg along with a significant reduction in oxidative stress as compared to criton X-100 treated control. Activated partial thromboplastin and prothrombin times were prolonged at all doses, while plasma fibrinogen level remained unaffected. Metformin pre-treatment also reduced endothelial cell damage in ferrous chloride induced thrombosis in carotid arteries. Thus, the results indicate a potential protective effect of metformin on atherothrombotic risk factors, as evident from an improvement in lipid profile, reduction in oxidative stress and thrombotic events.
    European journal of pharmacology 04/2011; 659(2-3):213-23. DOI:10.1016/j.ejphar.2011.03.029 · 2.53 Impact Factor
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    • "Fluorescent oxidation products in human plasma may represent a more global marker of oxidative stress for epidemiologic studies reflecting stable protein oxidation, advanced glycation end products, and advanced lipoxidation end products (e.g., malondialdehyde; Wu et al. 2007a). They have been associated with risk of coronary artery disease and they were associated with several known promoters of oxidative stress such as smoking and hypertension (Wu et al. 2007b; Mezzetti et al. 2001). "
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    ABSTRACT: Chemical components of air pollutant exposures that induce oxidative stress and subsequent inflammation may be partly responsible for associations of cardiovascular morbidity and mortality with airborne particulate matter and combustion-related pollutant gasses. However, epidemiologic evidence regarding this is limited. An exposure-assessment approach is to measure the oxidative potential of particle mixtures because it is likely that hundreds of correlated chemicals are involved in overall effects of air pollution on health. Oxidative potential likely depends on particle composition and size distribution, especially ultrafine particle concentration, and on transition metals and certain semivolatile and volatile organic chemicals. For health effects, measuring systemic oxidative stress in the blood is one feasible approach, but there is no universal biomarker of oxidative stress and there are many potential target molecules (lipids, proteins, DNA, nitric oxide, etc.), which may be more or less suitable for specific study goals. Concurrent with the measurement of oxidative stress, it is important to measure gene and/or protein expression of endogenous antioxidant enzymes because they can modify relations between oxidative stress biomarkers and air pollutants. Conversely, the expression and activities of these enzymes are modified by oxidative stress. This interplay will likely determine the observed effects of air pollutants on systemic inflammatory and thrombotic mediators and related clinical outcomes. Studies are needed to assess the reliability and validity of oxidative stress biomarkers, evaluate differences in associations between oxidative stress biomarkers and various pollutant measurements (mass, chemical components, and oxidative potential), and evaluate impacts of antioxidant responses on these relations.
    Air Quality Atmosphere & Health 03/2011; 4(1):37-52. DOI:10.1007/s11869-010-0095-2 · 1.80 Impact Factor
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    ABSTRACT: Our objective was to investigate associations between adiposity measures (BMI, waist circumference, waist-to-hip ratio, waist-to-height ratio, and abdominal height) and biomarkers of oxidative stress (glutathione (GSH), GSH peroxidase (GSH-Px), vitamin C, thiobarbituric acid reactive substances (TBARS), and trolox equivalent antioxidant capacity (TEAC)) among police officers. This cross-sectional study included randomly selected police officers (43 policewomen; 67 policemen) from Buffalo, New York. Adiposity measures were performed using standardized methods. Biomarkers were measured on fasting blood specimens. An oxidative stress score (OSS) was created as a composite of the biomarkers. ANOVAs were used to compare mean levels of biomarkers across tertiles of the adiposity measures. Officers were 26- to 61-years old. GSH was inversely associated with waist circumference (trend P = 0.030) and waist-to-hip ratio (trend P = 0.026). GSH-Px was inversely associated with BMI (trend P = 0.004) and with waist-to-height ratio (trend P = 0.017). No associations were observed for TEAC, TBARS, or OSS with any adiposity measure. Significant interactions were observed by physical activity status for GSH with waist circumference and waist-to-hip ratio and for vitamin C with waist circumference, waist-to-hip and waist-to-height ratios. The above associations were inversely related only among officers who reported engaging in physical activity. Inverse associations were observed for BMI and waist circumference with GSH, but only among women; the interaction with gender was significant. Larger indices of adiposity were associated with increased levels of oxidative stress and decreased levels of antioxidant defense.
    Obesity 09/2008; 16(11):2489-97. DOI:10.1038/oby.2008.395 · 3.73 Impact Factor
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