| 1. |
- Andersson, Agneta, et al.
(author)
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Whole-grain foods do not affect insulin sensitivity or markers of lipid peroxidation and inflammation in healthy, moderately overweight subjects
- 2007
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In: Journal of Nutrition. - 0022-3166 .- 1541-6100. ; 137:6, s. 1401-1407
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Journal article (peer-reviewed)abstract
- High intakes of whole grain foods are inversely related to the incidence of coronary heart diseases and type 2 diabetes, but the mechanisms remain unclear. Our study aimed to evaluate the effects of a diet rich in whole grains compared with a diet containing the same amount of refined grains on insulin sensitivity and markers of lipid peroxidation and inflammation. In a randomized crossover study, 22 women and 8 men (BMI 28 +/- 2) were given either whole-grain or refined-grain products (3 bread slices, 2 crisp bread slices, 1 portion muesli, and 1 portion pasta) to include in their habitual daily diet for two 6-wk periods. Peripheral insulin sensitivity was determined by euglycemic hyperinsulinemic clamp tests. 8-Iso-prostaglandin F(2alpha) (8-iso PGF(2alpha)), an F(2)-isoprostane, was measured in the urine as a marker of lipid peroxidation, and highly sensitive C-reactive protein and IL-6 were analyzed in plasma as markers of inflammation. Peripheral insulin sensitivity [mg glucose . kg body wt(-1) . min(-1) per unit plasma insulin (mU/L) x 100] did not improve when subjects consumed whole-grain products (6.8 +/- 3.0 at baseline and 6.5 +/- 2.7 after 6 wk) or refined products (6.4 +/- 2.9 and 6.9 +/- 3.2, respectively) and there were no differences between the 2 periods. Whole-grain consumption also did not affect 8-iso-PGF(2alpha) in urine, IL-6 and C-reactive protein in plasma, blood pressure, or serum lipid concentrations. In conclusion, substitution of whole grains (mainly based on milled wheat) for refined-grain products in the habitual daily diet of healthy moderately overweight adults for 6-wk did not affect insulin sensitivity or markers of lipid peroxidation and inflammation.
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| 2. |
- Basu, Samar, et al.
(author)
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Bioaktiva isoprostaner : nya markörer för oxidativ stress och inflammationsrelaterade sjukdomar
- 2009
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In: Läkartidningen. - 0023-7205 .- 1652-7518. ; 106:5, s. 274-278
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Journal article (peer-reviewed)abstract
- Oxidativ stress (fria radikaler) tros vara orsaken till åldrande och flera sjukdomar, däri bland arterioskleros, men det har saknats en pålitlig metodik för att påvisa aktiviteten av fria radikaler in vivo. Här presenteras isoprostaner som nya och tillförlitliga markörer för mätning av oxidativ stress in vivo genom indirekt mätning av radikalreaktioner. Isoprostaner kan ses i ökad mängd vid flera sjukdomstillstånd som är associerade med oxidativ stress och inflammation, till exempel kardiovaskulära sjukdomar, sjukdomar som är associerade med en ökad kardiovaskulär risk samt lungsjukdomar. Mätning av isoprostaner kan vidare ge ökad kunskap om fria radikalers fysiologiska roll och antioxidanternas roll vid sjukdomar samt vara ett verktyg vid utveckling av nya läkemedel mot oxidativ stress.
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| 3. |
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| 4. |
- Basu, Samar
(author)
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F2-isoprostane induced prostaglandin formation in the rabbit
- 2006
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In: Free radical research. - : Informa Healthcare. - 1071-5762 .- 1029-2470. ; 40:3, s. 273-277
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Journal article (peer-reviewed)abstract
- F2-isoprostanes, non-enzymatic free radical mediated products of arachidonic acid, have shown to form during various oxidant stress status and have potent biological effects. This study investigates to what extent 8-iso-PGF2α (a major F2-isoprostane), a bioactive product of lipid peroxidation can modify endogenous prostaglandin F2α (PGF2α) formation since prostaglandins are inflammatory as well as potent vasoregulatory substances that modulate diverse important physiological functions, and also form during acute and chronic inflammation. An immediate appearance and disappearance of 8-iso-PGF2α was seen in both plasma and urine within a short interval after i.v. administration of 43 μg/kg of 8-iso-PGF2α to the rabbits. A successive but differential formation of PGF2α resulted in a rapid and pulsatile increase of plasma 15-keto-dihydro-PGF2α, a major metabolite of primary PGF2α. Later, this compound was excreted efficiently as intact compound into the urine during the 3 h of experiment. A 8-fold increase of PGF2α metabolite in plasma at 10 min and 12-fold increase in the urine at 30–60 after the i.v. administration of 8-iso-PGF2α was observed which continued throughout the 3 h of experiment. This observation suggests that pharmacologically administered or endogenously produced 8-iso-PGF2α during oxidant stress induces prostaglandin formation presumbly through the classical cyclooxygenase-catalysed arachidonic acid oxidation which might be inflammatory itself to the cells and exerts further vasoconstrictive effects.
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| 5. |
- Basu, Samar
(author)
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F2-isoprostanes in human health and diseases : from molecular mechanisms to clinical implications
- 2008
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In: Antioxidants and Redox Signaling. - : Mary Ann Liebert. - 1523-0864 .- 1557-7716. ; 10:8, s. 1405-1434
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Research review (peer-reviewed)abstract
- Oxidative stress is implicated as one of the major underlying mechanisms behind many acute and chronic diseases, and involved in normal aging. However, the measurement of free radicals or their end products is complicated. Thus, proof of association of free radicals in pathologic conditions has been absent. Isoprostanes are prostaglandin-like bioactive compounds that are biosynthesized in vivo independent of cyclooxygenases, principally through free-radical catalyzation of arachidonic acid. Isoprostanes are now considered to be reliable biomarkers of oxidative stress, as evidenced by an autonomous study organized recently by the National Institutes of Health (NIH) in the United States. A number of these compounds have potent biologic activities such as vasoconstrictive and certain inflammatory properties. Isoprostanes are involved in many human diseases. Additionally, elevated levels of F2-isoprostanes have been seen in normal human pregnancy and after intake of some fatty acids, but their physiologic assignments have not yet been distinctive. This evidence indicates that measurement of bioactive F2-isoprostanes in body fluids offers a unique noninvasive analytic utensil to study the role of free radicals in physiology, oxidative stress–related diseases, experimental acute or chronic inflammatory conditions, and also in the assessment of various antioxidants, radical scavengers, and drugs.
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| 6. |
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| 7. |
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| 8. |
- Basu, Samar
(author)
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Novel cyclooxygenase-catalyzed bioactive prostaglandin F-2 alpha from physiology to new principles in inflammation
- 2007
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In: Medicinal research reviews (Print). - : Wiley. - 0198-6325 .- 1098-1128. ; 27:4, s. 435-468
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Research review (peer-reviewed)abstract
- Prostaglandin F2 (PGF2), a foremost stable vasoactive cyclooxygenase (COX)-catalyzed prostaglandin, regulates a number of key physiological functions such as luteolysis, ovarian function, luteal maintenance of pregnancy, and parturition as a constitutive part of ongoing reproductive processes of the body. It has recently been implicated in the regulation of intricate pathophysiological processes, such as acute and chronic inflammation, cardiovascular and rheumatic diseases. Since the discovery of a second isoform of COXs, it has been shown that PGF2 can be formed in vivo from arachidonic acid through both isoforms of COXs, namely cyclooxygenase-1 (COX-1) and cyclooxygenase-2 (COX-2). Being synthesized in various parts of the body, it metabolizes instantly to a number of rather inactive metabolites mainly in the lungs, liver, kidney, and efficiently excretes into the urine. 15-Keto-dihydro-PGF2, a major stable metabolite of PGF2 that reflects in vivo PGF2 biosynthesis, is found in larger quantities than its parent compound in the circulation and urine in basal physiological conditions, with short-lived pulses during luteolysis, induced termination of pregnancy and parturition, and is increased in tissues and various body fluids during acute, sub-chronic, and severe chronic inflammation. Further, the close relationship of PGF2 with a number of risk factors for atherosclerosis indicates its major role in inflammation pathology. This review addresses multiple aspects of PGF2 in addition to its emerging role in physiology to inflammation.
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| 9. |
- Basu, Samar, et al.
(author)
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Regulatory factors of basal F(2)-isoprostane formation: population, age, gender and smoking habits in humans.
- 2009
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In: Free radical research. - : Informa UK Limited. - 1029-2470 .- 1071-5762. ; 43:1, s. 85-91
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Journal article (peer-reviewed)abstract
- Oxidative stress is assumed to be the key underlying factor in the pathogenesis of many common diseases. This study describes the basal levels of 8-iso-PGF(2alpha ), a major F(2)-isoprostane and an in vivo oxidative stress biomarker in healthy subjects from three countries, namely Italy, Poland and Sweden, in relation to their smoking habits, age and gender. It studied urinary 8-iso-PGF(2alpha ) in 588 subjects from Sweden (n=220), Italy (n=203) and Poland (n=165). Polish subjects had the highest levels of F(2)-isoprostanes followed by the Swedish and Italians when adjusted for smoking, age, sex and creatinine and the inter-country differences were statistically significant. Smokers had significantly higher levels of 8-iso-PGF(2alpha ) compared to non-smokers in all countries and there was a moderate decrease with age. Women had only slightly lower 8-iso-PGF(2alpha ) than men. There is a difference in F(2)-isoprostane levels in vivo between countries. Smoking, age and gender affect isoprostane formation and should be taken into consideration in clinical studies of oxidative stress.
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| 10. |
- Basu, Samar
(author)
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The enigma of in vivo oxidative stress assessment: isoprostanes as an emerging target
- 2007
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In: Scandinavian Journal of Food & Nutrition. - : Informa UK Limited. - 1748-2984 .- 1748-2976. ; 51:2, s. 48-61
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Journal article (peer-reviewed)abstract
- Oxidative stress is believed to be one of the major factors behind several acute and chronic diseases, and may also be associated with ageing. Excess formation of free radicals in miscellaneous body environment may originate from endogenous response to cell injury, but also from exposure to a number of exogenous toxins. When the antioxidant defence system is overwhelmed, this leads to cell damage. However, the measurement of free radicals or their endproducts is tricky, since these compounds are reactive and short lived, and have diverse characteristics. Specific evidence for the involvement of free radicals in pathological situations has been difficult to obtain, partly owing to shortcomings in earlier described methods for the measurement of oxidative stress. Isoprostanes, which are prostaglandin-like bioactive compounds synthesized in vivo from oxidation of arachidonic acid, independently of cyclooxygenases, are involved in many human diseases, and their measurement therefore offers a way to assess oxidative stress. Elevated levels of F2-isoprostanes have also been seen in the normal human pregnancy, but their physiological role has not yet been defined. Large amounts of bioactive F2-isoprostanes are excreted in the urine in normal basal situations, with a wide interindividual variation. Their exact role in the regulation of normal physiological functions, however, needs to be explored further. Current understanding suggests that measurement of F2-isoprostanes in body fluids provides a reliable analytical tool to study oxidative stress-related diseases and experimental inflammatory conditions, and also in the evaluation of various dietary antioxidants, as well as drugs with radical-scavenging properties. However, assessment of isoprostanes in plasma or urine does not necessarily reflect any specific tissue damage, nor does it provide information on the oxidation of lipids other than arachidonic acid.
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| 11. |
- Basu, Samar, et al.
(author)
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Time course and attenuation of ischaemia-reperfusion induced oxidative injury by propofol in human renal transplantation
- 2007
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In: Redox report. - 1351-0002 .- 1743-2928. ; 12:4, s. 195-202
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Journal article (peer-reviewed)abstract
- Ischaemia-reperfusion injury resulting from interruption and restoration of blood flow might be related to free radical mediated oxidative stress and inflammation, and subsequently to post-surgery related complications. We studied the impact of renal transplantation on oxidative stress and inflammation by measuring F2-isoprostanes and prostaglandin F2α, respectively, during transplantation and post-surgery. Additionally, due to earlier observations, two dissimilar anaesthetic agents (thiopentone and propofol) were compared to determine their antioxidative capacity rather than their anaesthetic properties. Blood samples were collected before, post-intubation, immediately, 30, 60,120, 240 min, and 12 and 24 h after reperfusion. Oxidative stress and inflammatory response were detected by measuring 8-iso-PGF2α (a major F2-isoprostane and a biomarker of oxidative stress) and 15-keto-dihydro-PGF2α (a major metabolite of PGF2α and a biomarker of COX-mediated inflammatory response), respectively. Reperfusion of the transplanted graft significantly increased plasma levels of 8-iso-PGF2α. PGF2α metabolite levels, although elevated, did not reach statistical significance. In addition, significantly lower levels of 8-iso-PGF2a were observed in the propofol group compared to the thiopentone group. Together, these findings underline an augmented oxidative stress activity following an inflammatory response after human renal transplantation. Furthermore, propofol a well-known anaesthetic, counteracted oxidative stress by lowering the formation of a major F2-isoprostane.
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| 12. |
- Basu, Samar, et al.
(author)
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Type 1 diabetes is associated with increased cyclooxygenase- and cytokine-mediated inflammation
- 2005
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In: Diabetes Care. - : American Diabetes Association. - 0149-5992 .- 1935-5548. ; 28:6, s. 1371-1375
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Journal article (peer-reviewed)abstract
- OBJECTIVE: The extent of involvement of cyclooxygenase (COX)-mediated inflammation in type 1 diabetes is unknown, and the association between the COX- and cytokine-mediated inflammatory responses in type 1 diabetes is not fully understood. RESEARCH DESIGN AND METHODS: Plasma high-sensitivity C-reactive protein (CRP), 24-h urinary and plasma 15-keto-dihydro-prostaglandin F(2alpha) (a metabolite of prostaglandin F(2alpha) [PGF(2alpha)] and an indicator of COX-mediated inflammation), serum amyloid protein A (SAA), and interleukin (IL)-6 (indicators of inflammation) were measured in 38 subjects with type 1 diabetes and 41 healthy age- and sex-matched control subjects. RESULTS: The inflammatory indicators (urinary 15-keto-dihydro-PGF(2alpha), P < 0.01; IL-6, P < 0.04) were increased in men with diabetes. CRP and SAA did not show any significant difference between the diabetic and the control subjects. Urinary levels of 15-keto-dihydro-PGF(2alpha) correlated with the degree of glycemic control, HbA(1c) (r = 0.42, P < 0.0005). No correlation was found between the duration of diabetes and the inflammatory biomarkers or metabolic measurements. CONCLUSIONS: These results suggest that an early low-grade inflammatory process reflected by elevated levels of PGF(2alpha) and IL-6 is involved in type 1 diabetes. Thus, both COX- and cytokine-mediated inflammatory pathways are significantly related to type 1 diabetes.
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| 13. |
- Berg, K., et al.
(author)
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Oxidative stress during coronary artery bypass operations : Importance of surgical trauma and drug treatment
- 2006
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In: Scandinavian Cardiovascular Journal. - : Informa UK Limited. - 1401-7431 .- 1651-2006. ; 40:5, s. 291-297
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Journal article (peer-reviewed)abstract
- Objective. To investigate oxidative stress and myocardial injury at different stages of coronary artery bypass grafting (CABG). Design. Twenty patients underwent CABG with use of cardiopulmonary bypass (CPB) and with intermittent sampling of plasma and urine. Main markers were: 8-iso-PGF(2 alpha) (oxidative stress); troponin T (myocardial injury); and 15-keto-dihydro-PGF2 alpha and hsCRP (inflammation). Results. Plasma 8-iso-PGF2 alpha increased after start of surgery, but there was no further rise during CPB or after aortic cross-clamp release and no significant myocardial arterio-venous differences. An increase in troponin T was seen early after the operation, but no relationship was established between 8-iso-PGF2 alpha and troponin T. 8-iso-PGF2 alpha levels were elevated by preoperative withdrawal of acetylsalicylic acid (ASA) but reduced by intraoperative use of heparin. 15-keto-dihydro-PGF2 alpha was elevated during operation and hsCRP following operation. Conclusions. In the present study oxidative stress was multifactorial in origin with main impacts from surgical trauma, less from CPB and little if any from myocardial ischemia-reperfusion events. In addition, cardiovascular drugs in common use like ASA and heparin seemed to influence the pro- and antioxidant balance, a finding that has to be confirmed in future studies.
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| 14. |
- Bräsen, Jan Hinrich, et al.
(author)
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Extracellular superoxide dismutase accelerates endothelial recovery and inhibits in-stent restenosis in stented atherosclerotic Watanabe heritable hyperlipidemic rabbit aorta
- 2007
-
In: Journal of the American College of Cardiology. - : Elsevier BV. - 0735-1097 .- 1558-3597. ; 50:23, s. 2249-2253
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Journal article (peer-reviewed)abstract
- This study examined whether local gene therapy with extracellular superoxide dismutase (EC-SOD) could inhibit in-stent restenosis in atherosclerotic Watanabe heritable hyperlipidemic rabbits. Background Stenting causes an acute increase in superoxide anion production and oxidative stress; EC-SOD is a major component of antioxidative defense in blood vessels and has powerful cardioprotective effects in ischemic myocardium. Methods Endothelial denudation and stenting were done in 36 adult (15 to 18 months old) rabbits. Catheter-mediated intramural delivery of clinical good manufacturing practice-grade adenoviruses encoding rabbit EC-SOD were done simultaneously with stenting. Control animals received adenovirus-encoding nuclear-targeted β-galactosidase (AdLacZ). Circulating markers for oxidative stress (nonesterified 8-iso-prostaglandin F2 alpha) were measured. Analysis of 6-day, 28-day, and 90-day vessel histology, radical production, oxidation-specific epitopes, and expression studies were performed. Results The EC-SOD treatment reduced oxidant production in stented vessels compared with control vessels. Early systemic recovery of total SOD activity was observed in the treated rabbits. The EC-SOD significantly accelerated endothelial recovery (67.4% ± 10.8% vs. 24.2.1% ± 4.6% at 6 days, p < 0.05; 89.3% ± 3.7% vs. 45.1% ± 9.6% at 28 days, p < 0.05), and the beneficial effect involved increased proliferation of regenerating endothelium. The EC-SOD group showed a 61.3% lower (p < 0.05) neointimal formation at 28 days, with a similar, albeit nonsignificant trend at 90 days (1.20 ± 0.32 mm2 vs. 1.88 ± 0.24 mm2, p = 0.06). Conclusions The results suggest a central pathogenetic role of oxidation sensitive signaling processes in endothelial recovery and developing in-stent restenosis in atherosclerotic vessels. Local therapy against oxidative stress represents a promising therapeutic strategy in stent-induced vascular injury. Extracellular Superoxide Dismutase Accelerates Endothelial Recovery and Inhibits In-Stent Restenosis in Stented Atherosclerotic Watanabe Heritable Hyperlipidemic Rabbit Aorta Jan Hinrich Bräsen, Olli Leppänen, Matias Inkala, Tommi Heikura, Max Levin, Fabian Ahrens, Juha Rutanen, Hubertus Pietsch, David Bergqvist, Anna-Liisa Levonen, Samar Basu, Thomas Zeller, Günter Klöppel, Mikko O. Laukkanen, Seppo Ylä-Herttuala Percutaneous coronary interventions induce oxidative stress in vessels that already have compromised antioxidative defenses. Extracellular superoxide dismutase (EC-SOD) is a major antioxidant in healthy arteries, and exogenous EC-SOD confers powerful vasculoprotective and cardioprotective effects. However, the effects of EC-SOD therapy on stent-induced vascular injury have not been assessed. We present evidence showing that local therapy with EC-SOD, delivered using clinical-grade adenoviruses, attenuated tissue oxidant production, suppressed developing in-stent restenosis, and accelerated endothelial recovery.
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| 15. |
- Bräuner, Elvira Vaclavik, et al.
(author)
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Indoor particles affect vascular function in the aged: an air filtration-based intervention study.
- 2008
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In: American journal of respiratory and critical care medicine. - 1535-4970. ; 177:4, s. 419-25
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Journal article (peer-reviewed)abstract
- RATIONALE: Exposure to particulate matter is associated with risk of cardiovascular events, possibly through endothelial dysfunction, and indoor air may be most important. OBJECTIVES: We investigated effects of controlled exposure to indoor air particles on microvascular function (MVF) as the primary endpoint and biomarkers of inflammation and oxidative stress as secondary endpoints in a healthy elderly population. METHODS: A total of 21 nonsmoking couples participated in a randomized, double-blind, crossover study with two consecutive 48-hour exposures to either particle-filtered or nonfiltered air (2,533-4,058 and 7,718-12,988 particles/cm(3), respectively) in their homes. MEASUREMENTS AND MAIN RESULTS: MVF was assessed noninvasively by measuring digital peripheral artery tone after arm ischemia. Secondary endpoints included hemoglobin, red blood cells, platelet count, coagulation factors, P-selectin, plasma amyloid A, C-reactive protein, fibrinogen, IL-6, tumor necrosis factor-alpha, protein oxidation measured as 2-aminoadipic semialdehyde in plasma, urinary 8-iso-prostaglandin F(2alpha), and blood pressure. Indoor air filtration significantly improved MVF by 8.1% (95% confidence interval, 0.4-16.3%), and the particulate matter (diameter < 2.5 mum) mass of the indoor particles was more important than the total number concentration (10-700 nm) for these effects. MVF was significantly associated with personal exposure to iron, potassium, copper, zinc, arsenic, and lead in the fine fraction. After Bonferroni correction, none of the secondary biomarkers changed significantly. CONCLUSIONS: Reduction of particle exposure by filtration of recirculated indoor air for only 48 hours improved MVF in healthy elderly citizens, suggesting that this may be a feasible way of reducing the risk of cardiovascular disease.
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| 16. |
- Casadesus, Gemma, et al.
(author)
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Increased isoprostane and prostaglandin are prominent in neurons in Alzheimer disease
- 2007
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In: Molecular Neurodegeneration. - : Springer Science and Business Media LLC. - 1750-1326. ; 2:1, s. 2-
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Journal article (peer-reviewed)abstract
- BackgroundInflammation and oxidative stress are both involved in the pathogenesis of Alzheimer disease and have been shown to be reciprocally linked. One group of molecules that have been directly associated with inflammation and the production of free radicals are the prostaglandin 13,14-dihydro 15-keto PGF2α and the isoprostane 8-iso-PGF2α.ResultsTo further delineate the role of inflammatory and oxidative parameters in Alzheimer disease, in this study we evaluated the amount and localization of 13,14-dihydro 15-keto PGF2α and 8-iso-PGF2α in hippocampal post mortem tissue samples from age-matched Alzheimer disease and control patients. Our results demonstrate increased levels of 13,14-dihydro 15-keto PGF2α and 8-iso-PGF2α in the hippocampal pyramidal neurons of Alzheimer disease patients when compared to control patients.ConclusionThese data not only support the shared mechanistic involvement of free radical damage and inflammation in Alzheimer disease, but also indicate that multiple pathogenic "hits" are likely necessary for both the development and propagation of Alzheimer disease.
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| 17. |
- Daryani, Achraf, et al.
(author)
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Antioxidant intake, oxidative stress and inflammation among immigrant women from the Middle East living in Sweden : associations with cardiovascular risk factors
- 2007
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In: NMCD. Nutrition Metabolism and Cardiovascular Diseases. - : Elsevier BV. - 0939-4753 .- 1590-3729. ; 17:10, s. 748-756
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Journal article (peer-reviewed)abstract
- Background and aims: Immigrant women from the Middle East have higher cardiovascular risk compared to native women. Whether low antioxidant intake, oxidative stress or inflammation contributes to risk is unknown. In a cross-sectional study of 157 randomly selected foreign-born women (Iranian and Turkish) and native women living in Sweden, we investigated antioxidant status, oxidative stress (F-2-isoprostanes) and systemic inflammation (plasma high sensitive C-reactive protein; CRP) markers. We also investigated relationships between F2-isoprostanes, CRP and cardiovascular risk factors. Methods and result: Dietary intake was assessed using 24-h dietary recalls repeated four times. Micronutrient intake was not consistently different between groups. Serum a-tocopherol, but not gamma-tocopherot levels, was tower in Turkish vs. Swedish women (P < 0.05). Turkish women had the highest F-2-isoprostane levels (P < 0.05 vs. Iranian women) and CRP levels (P < 0.01 vs. Swedish women and P = 0.05 vs. Iranian women). In immigrants (n = 97), F-2-isoprostanes correlated positively to insulin levels (r = 0.31, P < 0.01), and CRP was correlated to obesity and several cardiovascular risk factors (r-values >0.21, P values <0.05). Conclusion: The rote of antioxidant status is unclear, whereas signs of oxidative stress and inflammation are evident in immigrant women from Middle East, especially Turkish women. Oxidative stress and low-grade inflammation might contribute to the higher cardiovascular risk previously observed in immigrant women. Further larger studies adjusting for more potential confounders are motivated to confirm these results.
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| 18. |
- Dawczynski, Christine, et al.
(author)
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Long-term moderate intervention with n-3 long-chain PUFA-supplemented dairy products : effects on pathophysiological biomarkers in patients with rheumatoid arthritis
- 2009
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In: British Journal of Nutrition. - 0007-1145 .- 1475-2662. ; 101:10, s. 1517-1526
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Journal article (peer-reviewed)abstract
- n-3 long-chain PUFA (n-3 LC-PUFA) may improve cardiovascular and inflammatory diseases. The effects of n-3 LC-PUFA-supplemented dairy products on inflammation and immunological parameters, biomarkers of oxidative stress, serum lipids, and on disease activity were determined in patients with rheumatoid arthritis (RA). Forty-five subjects (forty-three females and two males) were randomly divided into two groups in a double-blind, placebo-controlled cross-over study. Both groups received placebo or verum products consecutively for 3 months with a 2-month washout phase between the two periods. Blood samples were taken at the beginning and at the end of each period. The dairy products generally improved serum lipids by increasing HDL and lowering lipoprotein it. The n-3 LC-PUFA supplements act to lower TAG. Additionally, a decreased lipopolysaccharide-stimulated cylo-oxygenase-2 expression was found in patients who had consumed the enriched dairy products. The majority of the CD analysed were not influenced, although n-3 LC-PUFA did suppress the immune response as lymphocytes and monocytes were found to be significantly decreased. The n-3 LC-PUFA did not increase the biomarkers of oxidative stress such as 8-iso-PGF(2 alpha), and 15-keto-dihydro PGF(2 alpha), and DNA damage like 7,8-dihydro-8-oxo-2'-deoxyguanosine. The long-term consumption of dairy products (2 x 12 weeks) diminished the excretion of hydroxypyridinium crosslinks, and favoured the diastolic blood pressure. The consumption of moderate doses of n-3 LC-PUFA in combination with dairy products did not improve the disease activity. However, there is evidence of cardioprotective effects. Furthermore, the long-term consumption of dairy products acts against the cartilage and bone destruction in RA.
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| 19. |
- Feairheller, Deborah L, et al.
(author)
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Exercise training, NADPH oxidase p22phox gene polymorphisms, and hypertension
- 2009
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In: Medicine & Science in Sports & Exercise. - 0195-9131 .- 1530-0315. ; 41:7, s. 1421-1428
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Journal article (peer-reviewed)abstract
- INTRODUCTION: Oxidative stress that is mediated through NADPH oxidase activity plays a role in the pathology of hypertension, and aerobic exercise training reduces NADPH oxidase activity. The involvement of genetic variation in the p22phox (CYBA) subunit genes in individual oxidative stress responses to aerobic exercise training has yet to be examined in Pre and Stage 1 hypertensives. METHODS: Ninety-four sedentary Pre and Stage 1 hypertensive adults underwent 6 months of aerobic exercise training at a level of 70% VO2max to determine whether the CYBA polymorphisms, C242T and A640G, were associated with changes in urinary 8-iso-prostaglandin F2alpha (8-iso-PGF2alpha), urinary nitric oxide metabolites (NOx), and plasma total antioxidant capacity (TAC). RESULTS: Demographic and subject characteristics were similar among genotype groups for both polymorphisms. At baseline, a significant (P = 0.03) difference among the C2424T genotype groups in 8-iso-PGF2alpha levels was detected, with the TT homozygotes having the lowest levels and the CC homozygotes having the highest levels. However, no differences were found at baseline between the A640G genotype groups. After 6 months of aerobic exercise training, there was a significant increase in VO2max (P < 0.0001) in the entire study population. In addition, there were significant increases in both urinary 8-iso-PGF2alpha (P = 0.002) and plasma TAC (P=0.03) levels and a significant decrease in endogenous urinary NOx (P < 0.0001). Overall, aerobic exercise training elicited no significant differences among genotype groups in either CYBA variant for any of the oxidative stress variables. CONCLUSIONS: We found that compared with CYBA polymorphisms C242T and A640G, it was aerobic exercise training that had the greatest influence on the selected biomarkers; furthermore, our results suggest that the C242T CYBA variant influences baseline levels of urinary 8-iso-PGF2alpha but not the aerobic exercise-induced responses.
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| 20. |
- Fenty-Stewart, Nicola, et al.
(author)
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Independent and combined influence of AGTR1 variants and aerobic exercise on oxidative stress in hypertensives
- 2009
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In: Blood Pressure. - : Informa UK Limited. - 0803-7051 .- 1651-1999. ; 18:4, s. 204-212
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Journal article (peer-reviewed)abstract
- Angiotensin II (AngII), via the AngII type 1 receptor (AT(1)R), contributes to oxidative stress. Aerobic exercise training (AEXT) reduces the risk of cardiovascular (CV) disease, presumably by reducing the grade of oxidative stress. We investigated the independent and combined influence of the AGTR1 A1166C and -825 T/A polymorphisms on oxidative stress and plasma AngII responses to AEXT in pre- and stage 1 hypertensives. Urinary 8-iso-PGF(2alpha) significantly increased with AEXT (p=0.002); however, there were no significant changes in superoxide dismutase activity or AngII levels. There was a significant difference in the change in AngII levels with AEXT between A1166C genotype groups (p=0.04) resulting in a significant interactive effect of the A1166C polymorphism and AEXT on the change in AngII (p<0.05). Only the TT genotype group of the -825 T/A polymorphism had a significant reduction in plasma AngII (p=0.02). Risk allele analysis revealed a significant reduction in plasma AngII (p=0.04) and a significant increase in urinary 8-iso-PGF(2alpha) (p=0.01) with AEXT in individuals with two risk alleles only. Our findings suggest that variation in the AGTR1 gene is associated with differential changes in plasma AngII but not oxidative stress.
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| 21. |
- Fischer, C.P, et al.
(author)
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Vitamin E isoform-specific inhibition of the exercise-induced heat shock protein 72 expression in humans
- 2006
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In: Journal of applied physiology. - : American Physiological Society. - 8750-7587 .- 1522-1601. ; 100:5, s. 1679-1687
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Journal article (peer-reviewed)abstract
- Increased levels of reactive oxygen and nitrogen species, as seen in response to exercise, challenge the cellular integrity. Important protective adaptive changes include induction of heat shock proteins (HSPs). We hypothesized that supplementation with antioxidant vitamins C (ascorbic acid) and E (tocopherol) would attenuate the exercise-induced increase of HSP72 in the skeletal muscle and in the circulation. Using randomization, we allocated 21 young men into three groups receiving one of the following oral supplementations: RRR-α-tocopherol 400 IU/ day + ascorbic acid (AA) 500 mg/day (CEα), RRR-α-tocopherol 290 IU/day + RRR-γ-tocopherol 130 IU/day + AA 500 mg/day (CEαγ), or placebo (Control). After 28 days of supplementation, the subjects performed 3 h of knee extensor exercise at 50% of the maximal power output. HSP72 mRNA and protein content was determined in muscle biopsies obtained from vastus lateralis at rest (0 h), postexercise (3 h), and after a 3-h recovery (6 h). In addition, blood was sampled for measurements of HSP72, α-tocopherol, γ-tocopherol, AA, and 8-isoprostaglandin-F2α (8-PGF2α). Postsupplementation, the groups differed with respect to plasma vitamin levels. The marker of lipid peroxidation, 8-iso-PGF2α, increased from 0 h to 3 h in all groups, however, markedly less (P < 0.05) in CEα. In Control, skeletal muscle HSP72 mRNA content increased 2.5-fold (P < 0.05) and serum HSP72 protein increased 4-fold (P < 0.05) in response to exercise, whereas a significant increase of skeletal muscle HSP72 protein content was not observed (P = 0.07). In CEα, skeletal muscle HSP72 mRNA, HSP72 protein, and serum HSP72 were not different from Control in response to exercise. In contrast, the effect of exercise on skeletal muscle HSP72 mRNA and protein, as well as circulating HSP72, was completely blunted in CEαγ. The results indicate that γ-tocopherol comprises a potent inhibitor of the exercise-induced increase of HSP72 in skeletal muscle as well as in the circulation.
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| 22. |
- Florvall, Gösta, et al.
(author)
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Apolipoprotein A1 Is a Stronger Prognostic Marker Than Are HDL and LDL Cholesterol for Cardiovascular Disease and Mortality in Elderly Men
- 2006
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In: The journals of gerontology. Series A, Biological sciences and medical sciences. - 1079-5006 .- 1758-535X. ; 61:12, s. 1262-1266
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Journal article (peer-reviewed)abstract
- The aim of this study was to compare apolipoprotein A1 (ApoA1) and B (ApoB) with high-density lipoprotein cholesterol (HDL-C) and low-density lipoprotein cholesterol (LDL-C) as markers for cardiovascular mortality and morbidity in elderly men. We analyzed serum ApoA1, ApoB, total cholesterol, HDL-C, and LDL-C in a group of 77-year-old men (n = 785). The results were correlated with data from the Swedish cause of death registry. Receiver-operating characteristic curves showed that, of the studied serum markers, ApoA1 was the best predictor for ischemic heart disease mortality (area under the curve = 0.724, 95% confidence interval, 0.691-0.755). There were also significant correlations between the apolipoproteins and other known risk markers for cardiovascular disease such as triglycerides, high-sensitivity C-reactive protein (hsCRP), and cystatin C. Serum ApoA1 is a better risk marker than are ApoB, ApoB/ApoA1 ratio, HDL-C, and LDL-C for cardiovascular disease and mortality in elderly men.
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| 23. |
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| 24. |
- Florvall, Gösta, et al.
(author)
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Microalbuminuria measured by three different methods, blood pressure and cardiovascular risk factors in elderly Swedish males
- 2008
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In: Analytical Chemistry Insights. - 1177-3901. ; 3, s. 69-74
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Journal article (peer-reviewed)abstract
- Microalbuminuria is associated with hypertension and is a strong risk factor for subsequent chronic disease, both renal and coronary heart disease (CHD), Presently there are several methods available for measurement of microalbuminuria. The aim of this study was to evaluate if the three different methods gave similar information or if one of the assays were superior to the others. Blood pressure, infl ammatory markers and cardiovascular mortality and morbidity were correlated with urine albumin analysed with a point-of-care testing (POCT) instrument, nephelometric determination of albumin and albumin/creatinine ratio in elderly males. The study population consisted of 103 diabetic and 603 nondiabetic males (age 77 years) in a cross-sectional study. We analyzed urine albumin with a HemoCue® Urine Albumin POCT instrument and a ProSpec® nephelometer and albumin/creatinine ratio. There were strong correlations between both systolic and diastolic blood pressure and all three urine albumin methods (p < 0.0001). There were also signifi cant correlations between the different urine albumin measurements and serum amyloid A component, high-sensitivity C-reactive protein and interleukin-6. The three different urine albumin methods studied provided similar information in relation to cardiovascular disease. There was a strong correlation between systolic and diastolic blood pressure and microalbuminuria in both the whole study population and in nondiabetic males emphasizing the role of hypertension in glomerular damage. The good correlation between the studied urine albumin measurements show that all three methods can be used for monitoring urine albumin excretion.
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| 25. |
- Guron, Gregor, 1967, et al.
(author)
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Acute effects of the superoxide dismutase mimetic tempol on split kidney function in two-kidney one-clip hypertensive rats.
- 2006
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In: Journal of hypertension. - : Ovid Technologies (Wolters Kluwer Health). - 0263-6352. ; 24:2, s. 387-94
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Journal article (peer-reviewed)abstract
- OBJECTIVE: To investigate the acute effects of the superoxide dismutase mimetic 4-hydroxy-2,2,6,6-tetramethylpiperidine-1-oxyl (tempol) on split kidney function, and renal haemodynamics, in two-kidney, one-clip (2K1C) hypertensive rats. METHODS: Three weeks after clipping, or the sham procedure, the effects of intravenous tempol (200 micromol/kg per h) were evaluated on thiobutabarbital anaesthetized Sprague-Dawley rats. RESULTS: Mean arterial pressure (MAP; 152 +/- 3 versus 122 +/- 3 mmHg, P < 0.001), plasma renin activity (28.7 +/- 3.0 versus 9.5 +/- 0.6 ng/ml per h, P < 0.001) and urinary 8-iso-prostaglandin F2alpha excretion (124 +/- 4 versus 92 +/- 10 pmol/24 h, P = 0.003) were significantly elevated in 2K1C rats compared with sham. Tempol reduced MAP by 15 +/- 1% compared with baseline (P < 0.001) in 2K1C rats. In clipped kidneys, tempol increased the glomerular filtration rate (GFR; +50 +/- 15% from baseline) and the effective renal plasma flow (ERPF; +37 +/- 13%, from baseline), and reduced renal vascular resistance (RVR; -32 +/- 6% from baseline) compared with saline-treated controls (P < 0.05). In non-clipped kidneys, tempol reduced RVR (-24 +/- 5% from baseline) compared with saline-treated controls (P = 0.001). In sham-operated rats, tempol produced a modest reduction in MAP (-8 +/- 2% from baseline, P = 0.003), but did not significantly affect renal haemodynamics or function. CONCLUSION: Tempol reduced MAP and RVR in both clipped and non-clipped kidneys of 2K1C hypertensive rats. In addition, tempol increased ERPF and GFR in the clipped kidney. These findings suggest important roles for superoxide in the regulation of renal haemodynamics during the early maintenance phase of renovascular hypertension.
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