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1
Ramsey, K. H., I. M. Sigar, S. V. Rana, J. Gupta, S. M. Holland, G. I. Byrne, and J. D. Morrow. "Inducible Nitric Oxide Synthase Regulates Production of Isoprostanes In Vivo during Chlamydial Genital Infection in Mice." Infection and Immunity 71, no. 12 (December 2003): 7183–87. http://dx.doi.org/10.1128/iai.71.12.7183-7187.2003.
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ABSTRACT Urinary nitrite and F2-isoprostanes, an index of oxidant stress, were elevated during chlamydial genital infection of mice. Enhancement of urinary nitrite and F2-isoprostanes was observed in phagocyte oxidase-deficient mice. Inhibition of inducible nitric oxide synthase reduced isoprostane excretion. We conclude that nitrogen radicals induce F2-isoprostane production and excretion during murine chlamydial genital infection.
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Hermenegildo, Carlos, Marı́a Cinta Garcı́a-Martı́nez, Juan J. Tarı́n, and Antonio Cano. "Estradiol reduces F2α-isoprostane production in cultured human endothelial cells." American Journal of Physiology-Heart and Circulatory Physiology 283, no. 6 (December 1, 2002): H2644—H2649. http://dx.doi.org/10.1152/ajpheart.00369.2002.
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Free radical-generated F2α-isoprostanes are a group of compounds with vasoconstrictor properties. To investigate whether estradiol exerts antioxidant actions modifying F2α-isoprostane production, cultured human umbilical vein endothelial cells were exposed to estradiol and other compounds and F2α-isoprostanes were measured in culture medium. Exposure to 1 and 10 nM estradiol for 24 h reduced F2α-isoprostane production by 36 and 49%, respectively ( P < 0.001 vs. control). Exposure to antiestrogens alone (ICI-182780 or EM-652) slightly reduced F2α-isoprostanes ( P < 0.05 vs. control), but much less than exposure to estradiol ( P < 0.05). ICI-182780 reversed the estradiol-induced reduction of F2α-isoprostane concentration ( P < 0.05). Along with time-course analysis, these results suggest that estradiol effects were mediated through estrogen receptor-dependent and -independent mechanisms. Progestogens alone (progesterone or medroxyprogesterone acetate) did not modify F2α-isoprostane production at any of the tested concentrations (1, 10, and 100 nM). Progesterone completely reversed estradiol-induced reduction of F2α-isoprostane production ( P < 0.05 vs. control and estradiol), but medroxyprogesterone acetate did not ( P < 0.05 vs. control).
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Catalli, Adriana, Dawei Zhang, and Luke J. Janssen. "Receptors and signaling pathway underlying relaxations to isoprostanes in canine and porcine airway smooth muscle." American Journal of Physiology-Lung Cellular and Molecular Physiology 283, no. 5 (November 1, 2002): L1151—L1159. http://dx.doi.org/10.1152/ajplung.00038.2002.
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Using muscle bath techniques, we examined the inhibitory activities of several E- and F-ring isoprostanes in canine and porcine airway smooth muscle. 8-Isoprostaglandin E1 and 8-isoprostaglandin E2 (8-iso PGE2) reversed cholinergic tone in a concentration-dependent manner, whereas the F-ring isoprostanes were ineffective. Desensitization with 8-iso-PGE2 and PGE2 implicated isoprostane activity at the PGE2 receptor (EP). We found that the inhibitory E-ring isoprostane responses were significantly augmented by rolipram (a type IV phosphodiesterase inhibitor), while 1 H-[1,2,4]-oxadiazolo[4,3- a]quinoxalin-1-one (a guanylate cyclase inhibitor) had no effect, suggesting a role for cAMP in isoprostane-mediated relaxations. 8-Iso-PGE2 did not reverse KCl tone, suggesting that voltage-dependent Ca2+ influx and myosin light chain kinase are not suppressed by isoprostanes. Patch-clamp studies showed marked suppression of K+ currents by 8-iso-PGE2. We conclude that E-ring isoprostanes exert PGE2receptor-directed, cAMP-dependent relaxations in canine and porcine airway smooth muscle. This activity is not dependent on K+channel activation or the direct inhibition of voltage-operated Ca2+ influx or myosin light chain kinase.
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Rad, Esmaeil Yousefi, Ebrahim Falahi, Mahmoud Djalali, Amir Abbasnezhad, Mehdi Birjandi, and Somayeh Saboori. "Effect of Vitamin E Supplementation on Plasma and Urine Levels of Isoprostane F2α in Randomized Controlled Clinical Trials: A Systematic Review and Meta-Analysis." International Journal for Vitamin and Nutrition Research 87, no. 5-6 (September 1, 2017): 314–21. http://dx.doi.org/10.1024/0300-9831/a000488.
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Abstract. Vitamin E can reduce the level of lipid peroxidation and the related markers such as urine and plasma levels of isoprostanes. However, effects of vitamin E supplementation on plasma and urine level of isoprostane F2α as markers of lipid peroxidation were conflicting in various clinical trials. The current meta-analysis was carried out to determine the effects of vitamin E supplementation on plasma and urine levels of isoprostanes F2α in randomized clinical trials. A systematic search of RCTs was carried out in PubMed, Scopus, Science Direct and Cochrane Library databases. OF 889 relevantly founded articles, only four articles with five arms met the criteria for meta-analysis of plasma level of isoprostanes F2α. For the urine level of isoprostane F2α, three studies with 14 arms were included in the meta-analysis. After pooled analyzing, a significant reduction of 6.98 ng / l was seen in plasma level of isoprostane F2α in vitamin E receiving group (95% CI = -11.2, -2.76; P < 0.001) while no significant heterogeneity was seen between the studies included in this meta-analysis (P = 0.81 and I2 = 0.0%). However, the pooled effect of vitamin E supplementation on urine level of isoprostane F2α was not statistically significant (-11.31 pg / mg creatinine (95% CI = -26.4, 3.78; P = 0.88). Results of this meta-analysis have shown that vitamin E supplementation can only reduce plasma level of isoprostane F2α and has no significant effect on reducing urine level of this biomarker.
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Khitan, Zeid, Mohit Harsh, Komal Sodhi, Joseph I. Shapiro, and Nader G. Abraham. "HO-1 Upregulation Attenuates Adipocyte Dysfunction, Obesity, and Isoprostane Levels in Mice Fed High Fructose Diets." Journal of Nutrition and Metabolism 2014 (2014): 1–13. http://dx.doi.org/10.1155/2014/980547.
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Background.Fructose metabolism is an unregulated metabolic pathway and excessive fructose consumption is known to activate ROS. HO-1 is a potent antioxidant gene that plays a key role in decreasing ROS and isoprostanes. We examined whether the fructose-mediated increase in adipocyte dysfunction involves an increase in isoprostanes and that pharmacological induction of HO-1 would decrease both isoprostane levels and adipogenesis.Methods and Results.We examined the effect of fructose, on adipogenesis in human MSCs in the presence and absence of CoPP, an inducer of HO-1. Fructose increased adipogenesis and the number of large lipid droplets while decreasing the number of small lipid droplets (P<0.05). Levels of heme and isoprostane in fructose treated MSC-derived adipocytes were increased. CoPP reversed these effects and markedly increased HO-1 and the Wnt signaling pathway. The high fructose diet increased heme levels in adipose tissue and increased circulating isoprostane levels (P<0.05versus control). Fructose diets decreased HO-1 and adiponectin levels in adipose tissue. Induction of HO-1 by CoPP decreased isoprostane synthesis (P<0.05versus fructose).Conclusion.Fructose treatment resulted in increased isoprostane production and adipocyte dysfunction, which was reversed by the increased expression of HO-1.
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Devaraj, Sridevi, Shaina V. Hirany, Raymond F. Burk, and Ishwarlal Jialal. "Divergence between LDL Oxidative Susceptibility and Urinary F2-Isoprostanes as Measures of Oxidative Stress in Type 2 Diabetes." Clinical Chemistry 47, no. 11 (November 1, 2001): 1974–79. http://dx.doi.org/10.1093/clinchem/47.11.1974.
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Abstract Background: Oxidative stress is pivotal in atherogenesis. Although the most widely used indirect assay to quantify oxidative stress is LDL oxidative susceptibility, direct assays such as urinary F2-isoprostanes have shown great promise. Methods: We evaluated the utility of both a direct measure of oxidative stress (urinary F2-isoprostanes) and an indirect measure of copper-catalyzed, LDL oxidation in a model of increased oxidative stress (diabetes). We also evaluated an enzyme immunoassay (EIA) method for urinary F2-isoprostanes with a gas chromatography–mass spectrometry method. Results: Excellent intraassay and interassay CVs of <4% were obtained with our EIA method. A good correlation was obtained between the two methods (r = 0.80; n = 68) of F2-isoprostane measurement. An excellent correlation for F2-isoprostane concentrations was obtained between a timed collection vs 24-h urine (r = 0.96; n = 46). Baseline F2-isoprostane concentrations by EIA were significantly higher in both type 2 diabetics with and without macrovascular complications compared with controls (P <0.001). Supplementation with α-tocopherol led to a significant reduction in F2-isoprostane concentrations in all diabetic patients compared with baseline values (2.51 ± 1.76 compared with 1.69 ± 1.32 ng/mg creatinine; P <0.001). There were no significant differences in LDL oxidation in both diabetic groups compared with controls. α-Tocopherol supplementation led to significant increases in the lag phase of oxidation as measured by 3 indices in all groups. Conclusions: The measurement of urinary F2-isoprostanes provides a direct measure of in vivo lipid peroxidation and oxidative stress and appears to be superior to an indirect measure, e.g., LDL oxidative susceptibility, in type 2 diabetes.
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Il’yasova, Dora, Lynne E. Wagenknecht, Ivan Spasojevic, Steven Watkins, Donald Bowden, Frances Wang, and Ralph B. D’Agostino. "Urinary F2-Isoprostanes and Metabolic Markers of Fat Oxidation." Oxidative Medicine and Cellular Longevity 2015 (2015): 1–5. http://dx.doi.org/10.1155/2015/729191.
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Metabolomic studies of increased fat oxidation showed increase in circulating acylcarnitines C2, C8, C10, and C12 and decrease in C3, C4, and C5. We hypothesize that urinary F2-isoprostanes reflect intensity of fatty acid oxidation and are associated with circulating C2, C8, C10, and C12 directly and with C3, C4, and C5 inversely. Four urinary F2-isoprostane isomers and serum acylcarnitines are quantified using LC-MS/MS within the Insulin Resistance Atherosclerosis Study nondiabetic cohort (n= 682). Cross-sectional associations between fasting urinary F2-isoprostanes (summarized as a composite index) and the selected acylcarnitines are examined using generalized linear models. F2-isoprostane index is associated with C2 and C12 directly and with C5 inversely: the adjusted beta coefficients are 0.109, 0.072, and −0.094, respectively (P< 0.05). For these acylcarnitines and for F2-isoprostanes, the adjusted odds ratios (ORs) of incident diabetes are calculated from logistic regression models: the ORs (95% CI) are 0.77 (0.60–0.97), 0.79 (0.62–1.01), 1.18 (0.92–1.53), and 0.51 (0.35–0.76) for C2, C12, C5, and F2-isoprostanes, respectively. The direction of the associations between urinary F2-isoprostanes and three acylcarnitines (C2, C5, and C12) supports our hypothesis. The inverse associations of C2 and C12 and with incident diabetes are consistent with the suggested protective role of efficient fat oxidation.
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Salahudeen, A., K. Badr, J. Morrow, and J. Roberts. "Hydrogen peroxide induces 21-aminosteroid-inhibitable F2-isoprostane production and cytolysis in renal tubular epithelial cells." Journal of the American Society of Nephrology 6, no. 4 (October 1995): 1300–1303. http://dx.doi.org/10.1681/asn.v641300.
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F2-isoprostanes are the newly identified reactive oxygen species-catalyzed peroxidation products of arachidonate. The infusion of these prostaglandin F2-like prostanaoids into the rat kidney induces profound parallel reductions in RBF and GFR, suggesting that these metabolites may be partly responsible for the hemodynamic alterations seen in free radical-linked acute renal injury models. The present study examined directly in renal proximal tubular (LLC-PK1) cells whether hydrogen peroxide, a reactive oxygen species implicated in many models of acute renal injury, induces F2-isoprostane production and whether its production can be inhibited by the recently synthesized lipid peroxidation inhibitor 21-aminosteroid (lazaroid U-74389G). The incubation of LLC-PK1 cell layers with hydrogen peroxide for 3 h resulted in a dose-related six-fold increase in F2-isoprostane production, measured by the gas chromatographic-mass spectroscopic method. The preincubation of cells with 21-aminosteroid prevented hydrogen peroxide-induced F2-isoprostane production, a finding also demonstrable with other lipid peroxidation inhibitors, e.g., 2-methyl aminochroman (U-83836E) and diphenyl-p-phenylenediamine. Besides inhibiting isoprostane production, 21-aminosteroid reduced hydrogen peroxide-induced lipid degradation and peroxidation, and protected the cells against hydrogen peroxide-induced cytolysis. The novel finding that hydrogen peroxide induces 21-aminosteroid-inhibitable F2-isoprostane production in renal epithelial cells supports the in vivo report that its levels are elevated in reactive oxygen species-linked renal injury models such as ischemia-reperfusion. Besides direct cell injury, lipid peroxidation by generating F2-isoprostanes may further contribute to renal dysfunction through a vasoconstrictive mechanism. Thus, the inhibition of excess F2-isoprostane production may be one of the additional mechanisms, besides cytoprotection, by which antioxidants ameliorate renal dysfunction in experimental models of acute renal injury.
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Wiswedel, Ingrid, Daniela Peter, Andreas Gardemann, Francesco Carluccio, Hannelore Hampl, and Werner Siems. "Serum Concentrations of F2-Isoprostanes and 4-Hydroxynonenal in Hemodialysis Patients in Relation to Inflammation and Renal Anemia." Biomarker Insights 3 (January 2008): BMI.S363. http://dx.doi.org/10.4137/bmi.s363.
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Background Patients with end-stage renal disease (ESRD) undergoing hemodialysis (HD) are apparently exposed to enhanced oxidative stress and to inflammation. It was the aim of this study to characterize the state of systemic oxidative stress of ESRD patients before and following HD using highly specific biomarkers, F2-isoprostanes and 4-hydroxynonenal (HNE). Furthermore the question should be answered, if there are associations between inflammation and systemic oxidative stress and/or between systemic oxidative stress and renal anemia, which is more or less typical for HD patients. Patients and methods Concentrations of F2-isoprostanes, HNE, C-reactive protein (CRP) as marker of inflammation, and hemoglobin were measured in serum samples of patients with ESRD before and after HD and of healthy control persons for comparison. Total (esterified plus free) F2-isoprostanes were quantified by highly sensitive gas chromatography/mass spectrometry technique, HNE by thin layer chromatography and HPLC/UV detection, CRP by immunoturbidimetry and hemoglobin by clinico-chemical routine assay. Results 1. HD patients showed significantly higher serum concentrations of F2-isoprostanes and HNE than healthy human control subjects. 2. Total (esterified plus free) F2-isoprostane levels before HD were not significantly different from those after HD, whereas HNE levels were significantly decreased in patients after HD. 3. F2-isoprostane concentrations in HD patients correlated with the levels of CRP, whereas HNE concentrations inversely correlated with the content of hemoglobin. Conclusion Both, F2-isoprostanes and HNE serum concentrations are useful oxidative stress parameters in ESRD patients undergoing HD. Whereas HNE strongly correlates with the severity of renal anemia, leading to left heart insufficiency, F2-isoprostanes (sum of free plus esterified) highly correlate with the degree of inflammation.
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Awad, Joseph A., Jean-Louis Horn, L. Jackson Roberts II, and John J. Franks. "Demonstration of Halothane-induced Hepatic Lipid Peroxidation in Rats by Quantification of Flourine2-Isoprostanes." Anesthesiology 84, no. 4 (April 1, 1996): 910–16. http://dx.doi.org/10.1097/00000542-199604000-00019.
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Background Halothane can be reductively metabolized to free radical intermediates that may initiate lipid peroxidation. Hypoxia and phenobarbital pretreatment in Sprague-Dawley rats increases reductive metabolism of halothane. F(2)-isoprostanes, a novel measure of lipid peroxidation in vivo, were used to quantify halothane-induced lipid peroxidation in rats. Methods Rats were exposed to 1% halothane or 14% O(2) for 2 h. Pretreatments included phenobarbital, isoniazid, or vehicle. Rats also were exposed to halothane, enflurane, and desflurane at 21% O(2). Lipid peroxidation was assessed by mass spectrometric quantification of F(2)-isoprostanes. Results Exposure of phenobarbital-pretreated rats to 1% halothane at 21% O(2) for 2 h caused liver and plasma F(2)-isoprostane concentrations to increase fivefold compared to nonhalothane control rats. This halothane-induced increase was enhanced by 14% O(2), but hypoxia alone had no significant effect. Alanine aminotransferase activity at 24 h was significantly increased only in the 1% halothane/14% O(2) group. The effect of cytochrome P450 enzyme induction on halothane-induced F(2)-isoprostane production and liver injury was determined by comparing the effects of isoniazid and phenobarbital pretreatment with no pretreatment under hypoxic conditions. Halothane caused 4- and 11-fold increases in plasma and liver F(2)-isoprostanes, respectively, in non-pretreated rats, whereas isoniazid pretreatment had no effect. Phenobarbital pretreatment potentiated halothane-induced lipid peroxidation with 9- and 20-fold increases in plasma and liver F(2)-isoprostanes, respectively. Alanine aminotransferase activity was increased only in this group. At ambient oxygen concentrations, halothane but not enflurane or desflurane, caused F(2)-isoprostanes to increase. Conclusions Specific halothane-induced lipid peroxidation was demonstrated in Sprague-Dawley rats using quantification of F(2)-isoprostanes and was increased by hypoxia and phenobarbital pretreatment, but not isoniazid pretreatment.
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Nourooz-Zadeh, Jaffar. "Key issues in F2-isoprostane analysis." Biochemical Society Transactions 36, no. 5 (September 19, 2008): 1060–65. http://dx.doi.org/10.1042/bst0361060.
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A large body of evidence indicates that measurement of F2-isoprostanes, specific prostaglandin F2-like compounds derived from the non-enzymatic peroxidation of arachidonic acid, is a reliable biomarker of oxidant stress in the human body. Since the discovery of F2-isoprostanes in the early 1990s, a variety of analytical approaches has been introduced for the quantification of these novel compounds. The aim of the present review is to shed light on the available gas chromatographic–mass spectrometric assays for the measurement of plasma or urinary F2-isoprostanes and to highlight a number of issues which need to be addressed in order to implement F2-isoprostane measurement as a gold-standard biomarker of oxidative stress in biological samples.
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Widodo, Joko, Burhanuddin Bahar, and Mansyur Arif. "DAN MYELOPEROxIDASE) DAN DISFUNGSI ENDOTEL (ASIMETRIK DIMETILARGININ) DI KEGEMUKAN (OBESITAS)." INDONESIAN JOURNAL OF CLINICAL PATHOLOGY AND MEDICAL LABORATORY 16, no. 3 (March 17, 2018): 128. http://dx.doi.org/10.24293/ijcpml.v16i3.1039.
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Obesity is a pathological condition in which there is an excess body fat due to imbalance energy expenditure. Its association with oxidative stress could cause other metabolic disorders such as endothelial dysfunction, atherosclerosis, and cardiovascular disease. Theaim of this study was to assess the correlation of oxidative stress (F2-Isoprostane, Superoxide dismutase and Myeloperoxidase) andendothelial dysfunction (Asymmetric dimethylarginine) which happened in central obese men. A cross sectional study was carried outin 62 central obesity male subjects with ages range between 30−60 years. The researcher determined SOD activity, concentration ofMPO as well as ADMA. In this study was found a significant correlation of F2-Isoprostan (r = 0.333, p = 0.008), MPO (r = 0.386; p = 0.008) and ADMA but not with SOD. The elevated concentration of F2-Isoprostane occur 3.5 times (p = 0.02; 95%; CI = 1.19–10.19), elevated MPO occur 3.7 times (p = 0.023; 95%; CI = 1.16–11.56) while combination of elevated F2-Isoprostane-MPO occur6.7 times (p = 0.011; 95%; CI = 1.33-33.24) will increase the risk of endothelial dysfunction. There was a significant correlation of oxidative stress with endothelial dysfunction, and the increase concentration of F2-Isoprostane and MPO indicates the occurrence of endothelial dysfunction in central obesity.
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Shoman, Yara, Pascal Wild, Maud Hemmendinger, Melanie Graille, Jean-Jacques Sauvain, Nancy B. Hopf, and Irina Guseva Canu. "Reference Ranges of 8-Isoprostane Concentrations in Exhaled Breath Condensate (EBC): A Systematic Review and Meta-Analysis." International Journal of Molecular Sciences 21, no. 11 (May 28, 2020): 3822. http://dx.doi.org/10.3390/ijms21113822.
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Isoprostanes are physiopathologic mediators of oxidative stress, resulting in lipid peroxidation. 8-isoprostane seems particularly useful for measuring oxidative stress damage. However, no reference range values are available for 8-isoprosante in exhaled breath condensate (EBC) of healthy adults, enabling its meaningful interpretation as a biomarker. We conducted this systematic review and meta-analysis according to the protocol following PROSPERO (CRD42020146623). After searching and analyzing the literature, we included 86 studies. After their qualitative synthesis and risk of bias assessment, 52 studies were included in meta-analysis. The latter focused on studies using immunological analytical methods and investigated how the concentrations of 8-isoprostane differ based on gender. We found that gender had no significant effect in 8-isoprostane concentration. Among other studied factors, such as individual characteristics and factors related to EBC collection, only the device used for EBC collection significantly affected measured 8-isoprostane concentrations. However, adjustment for the factors related to EBC collection, yielded uncertainty whether this effect is due to the device itself or to the other factors. Given this uncertainty, we estimated the reference range values of 8-isoprostane stratified by gender and EBC collection device. A better standardization of EBC collection seems necessary; as well more studies using chemical analytical methods to extend this investigation.
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Iuliano, Luigi, Domenico Praticò, Domenico Ferro, Valerio Pittoni, Guido Valesini, John Lawson, Garret A. FitzGerald, and Francesco Violi. "Enhanced Lipid Peroxidation in Patients Positive for Antiphospholipid Antibodies." Blood 90, no. 10 (November 15, 1997): 3931–35. http://dx.doi.org/10.1182/blood.v90.10.3931.
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Abstract The mechanism leading to the formation of antiphospholipid antibodies (aPL) is still unknown. Because an in vitro study suggested that aPL may derive from pro-oxidant conditions, we sought a relationship between aPL and isoprostanes, indices of lipid peroxidation in vivo. Thirty patients with systemic lupus erythematosus have been studied. Seventeen (56.6%) were positive for aPL because they had lupus anticoagulant and/or high titer of anticardiolipin antibodies (aCL). Plasma levels of tumor necrosis factor (TNF ) and urinary excretion of two isoprostanes, 8-epi-PGF2α and IPF2α -I, free radical catalyzed oxidation products of arachidonic acid, were measured. Patients with systemic lupus erythematosus had higher urinary excretion of 8-epi-PGF2α and IPF2α -I than controls; urinary excretion of the two isoprostanes was highly correlated (Rho = 0.74, P < .0001). Urinary 8-epi-PGF2α was highly correlated with both aCL titer (Rho = 0.70, P < .0001) and TNF (Rho = 0.84, P < .0001), a measure of disease severity. Excretion of this isoprostane was also higher in those patients who exhibited aPL (P < .0001). Comparable correlations were observed with the isoprostane IPF2α -I. No difference of 8-epi-PGF2α was observed between patients with and without previous history of thrombosis. This study, showing the existence of a close association between aPL and increased in vivo lipid peroxidation, supports the hypothesis that these antibodies may result from pro-oxidative conditions and suggests that inflammation may play an important role.
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Anderson, Chelsea, Ginger L. Milne, Dale P. Sandler, and Hazel B. Nichols. "Oxidative stress in relation to diet and physical activity among premenopausal women." British Journal of Nutrition 116, no. 8 (October 11, 2016): 1416–24. http://dx.doi.org/10.1017/s0007114516003226.
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AbstractHigher levels of oxidative stress, as measured by F2-isoprostanes, have been associated with chronic diseases such as CVD and some cancers. Improvements in diet and physical activity may help reduce oxidative stress; however, previous studies regarding associations between lifestyle factors and F2-isoprostane concentrations have been inconsistent. The aim of this cross-sectional study was to investigate whether physical activity and intakes of fruits/vegetables, antioxidant nutrients, dietary fat subgroups and alcohol are associated with concentrations of F2-isoprostane and the major F2-isoprostane metabolite. Urinary F2-isoprostane and its metabolite were measured in urine samples collected at enrolment from 912 premenopausal women (aged 35–54 years) participating in the Sister Study. Physical activity, alcohol consumption and dietary intakes were self-reported via questionnaires. With adjustment for potential confounders, the geometric means of F2-isoprostane and its metabolite were calculated according to quartiles of dietary intakes, alcohol consumption and physical activity, and linear regression models were used to evaluate trends. Significant inverse associations were found between F2-isoprostane and/or its metabolite and physical activity, vegetables, fruits, vitamin C, α-carotene, vitamin E, β-carotene, vitamin A, Se, lutein+zeaxanthin and long-chain n-3 fatty acids. Although trans fats were positively associated with both F2-isoprostane and its metabolite, other dietary fat subgroups including SFA, n-6 fatty acids, n-3 fatty acids, MUFA, PUFA, short-chain n-3 fatty acids, long-chain n-3 fatty acids and total fat were not associated with either F2-isoprostane or its metabolite. Our findings suggest that lower intake of antioxidant nutrients and higher intake of trans fats may be associated with greater oxidative stress among premenopausal women.
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Andrianjafimasy, Miora, Farid Zerimech, Zeina Akiki, Helene Huyvaert, Nicole Le Moual, Valérie Siroux, Régis Matran, Orianne Dumas, and Rachel Nadif. "Oxidative stress biomarkers and asthma characteristics in adults of the EGEA study." European Respiratory Journal 50, no. 6 (December 2017): 1701193. http://dx.doi.org/10.1183/13993003.01193-2017.
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Asthma is an oxidative stress related disease, but associations with asthma outcomes are poorly studied in adults. We aimed to study the associations between several biomarkers related to oxidative stress and various asthma outcomes.Cross-sectional analyses were conducted in 1388 adults (mean age 43 years, 44% with asthma) from the Epidemiological Study of the Genetics and Environment of Asthma (EGEA2). Three blood antioxidant enzyme activities (biomarkers of response to oxidative stress) and exhaled breath condensate 8-isoprostanes and plasma fluorescent oxidation products (FlOPs) levels (two biomarkers of damage) were measured. Associations between biomarkers and 1) ever asthma and 2) asthma attacks, asthma control and lung function in participants with asthma were evaluated using regression models adjusted for age, sex and smoking.Biomarkers of response were unrelated to asthma outcomes. Higher 8-isoprostane levels were significantly associated with ever asthma (odds ratio for one interquartile range increase 1.28 (95% CI 1.06–1.67). Among participants with asthma, 8-isoprostane levels were negatively associated with adult-onset asthma (0.63, 0.41–0.97) and FlOPs levels were positively associated with asthma attacks (1.33, 1.07–1.65), poor asthma control (1.30, 1.02–1.66) and poor lung function (1.34, 1.04–1.74).Our results suggest that 8-isoprostanes are involved in childhood-onset asthma and FlOPs are linked to asthma expression.
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Vecchio, Daniela, Alessandra Acquaviva, Beatrice Arezzini, Hermann Tenor, Piero A. Martorana, and Concetta Gardi. "Downregulation of NOX4 Expression by Roflumilast N-Oxide Reduces Markers of Fibrosis in Lung Fibroblasts." Mediators of Inflammation 2013 (2013): 1–8. http://dx.doi.org/10.1155/2013/745984.
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The phosphodiesterase 4 inhibitor roflumilast prevents bleomycin- (BLM-) induced lung fibrosis in animal models. However, its mechanism of action remains unknown. We investigated whether roflumilast N-oxide (RNO), the active metabolite of roflumilast, can modulatein vitrothe oxidative effects of BLM on human lung fibroblasts (HLF). In addition, since BLM increases the production of F2-isoprostanes that haveper sefibrogenic activity, the effect of RNO on oxidative stress and fibrogenesis induced by the F2-isoprostane 8-epi-PGF2αwas investigated. HLF were preincubated either with the vehicle or with RNO and exposed to either BLM or 8-epi-PGF2α. Proliferation and collagen synthesis were assessed as [3H]-thymidine and [3H]-proline incorporation. Reactive oxygen species (ROS) and F2-isoprostanes were measured. NADPH oxidase 4 (NOX4) protein and mRNA were also evaluated. BLM increased both cell proliferation and collagen synthesis and enhanced ROS and F2-isoprostane production. These effects were significantly prevented by RNO. Also, RNO significantly reduced the increase in both NOX4 mRNA and protein, induced by BLM. Finally, 8-epi-PGF2α per sestimulated HLF proliferation, collagen synthesis, and NOX4 expression and ROS generation, and RNO prevented these effects. Thus, the antifibrotic effect of RNO observedin vivomay be related to its ability to mitigate ROS generation via downregulation of NOX4.
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Koregol, Arati C., Nagaraj B. Kalburgi, Sireesha kanniappa sadasivan, shivaraj warad, Apoorva kamat wagh, Tivin Thomas, and Priya sinha. "8-Isoprostane in chronic periodontitis and type II diabetes: Exploring the link." Journal of Dental Research, Dental Clinics, Dental Prospects 12, no. 4 (December 19, 2018): 252–57. http://dx.doi.org/10.15171/joddd.2018.039.
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Background. Reactive oxygen species (ROS) are associated with the pathogenesis of inflammatory diseases and have a direct or indirect role in tissue damage constituting oxidative stress. ROS are also involved in impairment of β-cell function during development of diabetes, which leads to genetic ablation of KATP channels, triggering up-regulation of antioxidant enzymes. Several markers of lipid peroxidation, protein oxidation and DNA damage induced by ROS can be measured. Over the last decade, isoprostanes have been considered as the best markers of lipid peroxidation. The aim of this study was to determine the presence of 8-isoprostane in healthy, chronic periodontitis and chronic periodontitis subjects with type II diabetes and to find the correlation between 8-isoprostane levels among groups and with clinical parameters like gingival index, probing depth and clinical attachment levels. Methods. Ninety subjects were selected and divided into 3 groups: healthy, chronic periodontitis and chronic periodontitis subjects with type II diabetes (n=30 each). Saliva was collected from these subjects after obtaining consent and analyzed for 8-isoprostane levels using ELISA kit. Statistical analysis was performed using Kruskal-Wallis test, Mann-Whitney U test and Spearman’s correlation coefficient (P<0.001). Results. Statistically significant difference was found in the levels of 8-isoprostane between healthy, chronic periodontitis and chronic periodontitis subjects with type II diabetes and with all clinical parameters. Conclusion. 8-isoprostane can be considered as a pathophysiological marker to measure oxidative stress in periodontal diseases.
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Sircar, Debajit, and Papasani V. Subbaiah. "Isoprostane Measurement in Plasma and Urine by Liquid Chromatography–Mass Spectrometry with One-Step Sample Preparation." Clinical Chemistry 53, no. 2 (February 1, 2007): 251–58. http://dx.doi.org/10.1373/clinchem.2006.074989.
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Abstract Background: Isoprostane F2α (iPF2α-III) concentration in plasma and urine is widely accepted as a measure of oxidative stress. Gas chromatography–mass spectrometry (GC/MS) methods for measuring iPF2α-III involve several steps of sample preparation and are labor-intensive, and ELISA methods, although easier to use, are less reliable. Therefore we developed a simple and sensitive method involving 1-step sample cleanup and HPLC/MS quantification. Methods: Samples of plasma or urine were enriched with a deuterated (iPF2α-III-D4) standard, treated with KOH to liberate the bound isoprostanes, then loaded onto an immunoaffinity column, and the bound isoprostane was eluted with 95% ethanol. The concentrated sample was injected onto a C-18 HPLC column, and the isoprostane was eluted with a gradient of acetonitrile in water and analyzed by electrospray negative ionization, selectively monitoring the ions 353.2 (iPF2α-III) and 357.2 (iPF2α-III-D4). The amount of isoprostane in the sample was calculated from the ratio of the intensities of the 2 ions. Results: The described method has a detection limit of 0.5 ng/L, with a linear dynamic range of 1–5000 ng/L. The intra- and interassay imprecisions were 4.68% and 3.88%, respectively. The values obtained correlated strongly with the GC/MS procedure (r = 0.80), but the absolute values were ∼4– to 5-fold lower, because the present method measures specifically 1 isomer of isoprostane, whereas the GC/MS method measures 4 isomers together. Conclusions: Because of its simplicity and lower limit of quantification, the present method provides a useful noninvasive tool for determining oxidative stress in patients.
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Salahudeen, A., V. Poovala, W. Parry, R. Pande, V. Kanji, N. Ansari, J. Morrow, and J. Roberts. "Cisplatin induces N-acetyl cysteine suppressible F2-isoprostane production and injury in renal tubular epithelial cells." Journal of the American Society of Nephrology 9, no. 8 (August 1998): 1448–55. http://dx.doi.org/10.1681/asn.v981448.
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In the low intracellular chloride milieu, chloride ions of cisplatin may exchange for cellular SH moieties resulting in glutathione depletion, H2O2 accumulation, and lipid peroxidation. Cisplatin-induced lipid peroxidation, in addition to causing direct cellular injury, may further contribute to cisplatin-induced renal dysfunction by generating vasoconstrictive E2- and F2-isoprostanes. The aim of this study was to determine whether cisplatin-induced renal epithelial (LLC-PK1 and primary human proximal tubular) cell injury is associated with increased production of isoprostanes, and whether this can be suppressed with a thiol donor, N-acetyl cysteine. It was confirmed that incubation of renal epithelial cells with cisplatin resulted in N-acetyl cysteine-inhibitable glutathione depletion, H2O2 accumulation, lipid degradation, and lactate dehydrogenase release. In additional experiments, incubation of cells with cisplatin for 48 h was accompanied by a dose-related increase in total (free plus esterified) F2-isoprostanes. An increase in F2-isoprostanes was discernible at 16.5 microM cisplatin and doubled at 66.0 microM. N-Acetyl cysteine at 50 microM concentration effectively suppressed 66.0 microM cisplatin-induced increase in isoprostanes. Similar findings were also obtained in human cells. Thus, cisplatin-induced tubular cell injury is accompanied by increased isoprostane production through a mechanism involving thiol depletion. On the basis of this new finding, it is hypothesized that these arachidonic acid peroxidation products may be partially responsible for the cisplatin-induced renal vasoconstriction demonstrable in the in vivo models.
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Feldo, Marcin, Michał Woźniak, Magdalena Wójciak-Kosior, Ireneusz Sowa, Agata Kot-Waśik, Justyna Aszyk, Jacek Bogucki, Tomasz Zubilewicz, and Anna Bogucka-Kocka. "Influence of Diosmin Treatment on the Level of Oxidative Stress Markers in Patients with Chronic Venous Insufficiency." Oxidative Medicine and Cellular Longevity 2018 (August 28, 2018): 1–5. http://dx.doi.org/10.1155/2018/2561705.
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Oxidative stress plays an important role in the pathophysiology of many human disorders, while antioxidants prevent the development of various adverse symptoms. Diosmin is a natural flavonoid applied in vascular system disorders, especially in chronic venous insufficiency (CVI), and it plays a significant part in the alleviation of CVI symptoms. Due to antioxidant activity, it also has the ability to scavenge the oxygen free radicals and hence decreases the level of oxidative stress biomarkers, such as prostaglandins and their precursors—isoprostanes. In the study, the influence of diosmin treatment on the level of isoprostanes in plasma samples of patients suffering from CVI was examined. The qualitative analysis was performed using high-performance liquid chromatography with spectrometry detection (LC-MS). The statistically significant decrease of isoprostane content after 3 months of treatment was observed within the studied group; however, the most significant changes were observed in patients who smoke.
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Long, Nancy C., Jung Suh, Jason D. Morrow, Robert H. Schiestl, G. G. Krishna Murthy, Joseph D. Brain, and Balz Frei. "Ozone causes lipid peroxidation but little antioxidant depletion in exercising and nonexercising hamsters." Journal of Applied Physiology 91, no. 4 (October 1, 2001): 1694–700. http://dx.doi.org/10.1152/jappl.2001.91.4.1694.
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Ozone (O3), a major component of urban air pollution, is a strong oxidizing agent that can cause lung injury and inflammation. In the present study, we investigated the effect of inhalation of O3 on levels of F2-isoprostanes in bronchoalveolar lavage fluid (BALF) and on levels of antioxidants in the BALF and plasma of hamsters. Because antioxidants, including urate, ascorbate, GSH, and vitamin E, defend the lungs by reacting with oxidizing agents, we expected to find a decrease in antioxidant levels after O3exposure. Similarly, we expected an increase in the levels of F2-isoprostanes, which are lipid peroxidation products. Exposure to 1.0 or 3.0 parts/million (ppm) O3 for 6 h resulted in an increase in BALF neutrophil numbers, an indicator of acute inflammation, as well as elevation of BALF F2-isoprostanes. The higher dose of O3 caused an increase in the BALF level of urate and a decrease in the plasma level of ascorbate, but 1.0 ppm O3 had no effect on BALF or plasma antioxidant levels. Exposure to 0.12 ppm O3 had no effect on BALF neutrophils or F2-isoprostanes nor on BALF and plasma antioxidants. We also investigated the effect of O3 exposure of hamsters during exercise on F2-isoprostane and antioxidant levels. We found that exposure to 1.0 ppm O3 during 1 h of exercise on a laddermill increased BALF levels of F2-isoprostanes but had no effect on BALF neutrophils or on BALF and plasma antioxidants. These results indicate that O3 induces inflammation and biomolecule oxidation in the lungs, whereas extracellular antioxidant levels are relatively unchanged.
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Gao, Ling, Huiyong Yin, Ginger L. Milne, Ned A. Porter, and Jason D. Morrow. "Formation of F-ring Isoprostane-like Compounds (F3-Isoprostanes)in Vivofrom Eicosapentaenoic Acid." Journal of Biological Chemistry 281, no. 20 (March 28, 2006): 14092–99. http://dx.doi.org/10.1074/jbc.m601035200.
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Pfister, Sandra L., Kasem Nithipatikom, and William B. Campbell. "Role of superoxide and thromboxane receptors in acute angiotensin II-induced vasoconstriction of rabbit vessels." American Journal of Physiology-Heart and Circulatory Physiology 300, no. 6 (June 2011): H2064—H2071. http://dx.doi.org/10.1152/ajpheart.01135.2010.
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This study explored the hypothesis that a portion of angiotensin II-induced contractions is dependent on superoxide generation and release of a previously unidentified arachidonic acid metabolite that activates vascular smooth muscle thromboxane receptors. Treatment of rabbit aorta or mesentery artery with the thromboxane receptor antagonist SQ29548 (10 μM) reduced angiotensin II-induced contractions (maximal contraction in aorta; control vs. SQ29548: 134 ± 16 vs. 93 ± 10%). A subset of rabbits deficient in vascular thromboxane receptors also displayed decreased contractions to angiotensin II. The superoxide dismutase mimetic Tiron (30 mM) attenuated angiotensin II-induced contractions only in rabbits with functional vascular thromboxane receptors (maximal contraction in aorta; control vs. Tiron: 105 ± 5 vs. 69 ± 11%). Removal of the endothelium or treatment with a nitric oxide synthase inhibitor, nitro-l-arginine (30 μM) did not alter angiotensin II-induced contractions. Tiron and SQ29548 decreased angiotensin II-induced contractions in the denuded aortas by a similar percentage as that observed in intact vessels. The cyclooxygenase inhibitor indomethacin (10 μM) or thromboxane synthase inhibitor dazoxiben (10 μM) had no effect on angiotensin II-induced contractions indicating that the vasoconstrictor was not thromboxane. Angiotensin II increased the formation of a 15-series isoprostane. Isoprostanes are free radical-derived products of arachidonic acid. The unidentified isoprostane increased when vessels were incubated with the superoxide-generating system xanthine/xanthine oxidase. Pretreatment of rabbit aorta with the isoprostane isolated from aortic incubations enhanced angiotensin II-induced contractions. Results suggest the factor activating thromboxane receptors and contributing to angiotensin II vasoconstriction involves the superoxide-mediated generation of a 15-series isoprostane.
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Gross, Myron, Michael Steffes, David R. Jacobs, Xinhua Yu, Linda Lewis, Cora E. Lewis, and Catherine M. Loria. "Plasma F2-Isoprostanes and Coronary Artery Calcification: The CARDIA Study." Clinical Chemistry 51, no. 1 (January 1, 2005): 125–31. http://dx.doi.org/10.1373/clinchem.2004.037630.
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Abstract Background: Oxidation of lipids in lipoproteins and cells may initiate and enhance the early development of cardiovascular disease. Method and Results: We assayed F2-isoprostanes, oxidation products of arachidonic acid, by gas chromatography–mass spectrometry in a biracial cohort of 2850 young healthy adult men and women. Coronary artery calcification (CAC), a component of coronary artery atherosclerosis, was detectable in 10% of the cohort and appeared to be in its initial stages (Agatston scores <20 in 47% and <100 in 83% of CAC-positive participants). After adjusting for sex, clinical site, age, and race, the presence of any CAC was 24% more likely among those with high vs low concentrations of F2-isoprostanes [odds ratio (OR) = 1.24 per 92.2 pmol/L (32.7 ng/L; 1 SD of F2-isoprostanes); 95% confidence interval (CI), 1.09–1.41]. The OR was only slightly attenuated [1.18 per 92.2 pmol/L (32.7 ng/L); CI, 1.02–1.38] after further adjustment for body mass index, smoking, serum lipids, C-reactive protein, antioxidant supplementation use, diabetes, and blood pressure. As a continuous variable, the Agatston score increased by 6.9% per 92.2 pmol/L (32.7 ng/L) of F2-isoprostane concentration (P <0.01). Whereas CAC prevalence was lower in women than men, mean (SD), F2-isoprostanes were higher in women {190 (108.9) pmol/L [67.4 (38.6) ng/L]} than in men {140.4 (55.6) pmol/L [49.8 (19.7) ng/L]}. Nevertheless, F2-isoprostanes were associated with an increased risk of CAC in both sexes. Conclusion: This association between increased concentrations of circulating F2-isoprostanes and CAC in young healthy adults supports the hypothesis that oxidative damage is involved in the early development of atherosclerosis.
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Teunissen, CE, M. Sombekke, L. van Winsen, J. Killestein, F. Barkhof, CH Polman, CD Dijkstra, MA Blankenstein, and D. Pratico. "Increased plasma 8,12-iso-iPF2alpha- VI levels in relapsing multiple sclerosis patients are not predictive of disease progression." Multiple Sclerosis Journal 18, no. 8 (June 13, 2012): 1092–98. http://dx.doi.org/10.1177/1352458511433306.
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Background: Oxidative stress plays an important role in multiple sclerosis (MS). Isoprostanes are biomarkers for oxidative stress and have been related to neurological disease progression. Objective: To study whether plasma isoprostane levels were related to disease progression in MS. Methods: Plasma levels of 8,12-iso-iPF2alpha-VI were determined in 17 patients with clinically isolated syndrome (CIS), 41 relapsing–remitting MS (RRMS) patients and 5 primary progressive MS (PPMS) patients and related to MRI and clinical disease parameters. Results: Isoprostane levels were similar in CIS (60.9, interquartile range (IQR): 47.7–77.7 pg/ml) and RRMS patients (65.3, IQR: 51.9–82.8 pg/ml). The plasma levels were lower in PPMS patients (42.5, IQR: 37.1–49.9) pg/ml, p<0.05) compared to CIS and RRMS patients in this cohort, which was not confirmed in a second cohort. Baseline isoprostane levels were not related to clinical progression defined by conversion form CIS to RRMS or change in Expanded Disability Status Scale (EDSS) or MS Functional Composite (MSFC) scores during six years of follow-up (CIS + RRMS), nor to change in volume of gadolinium enhancing lesions, T2 lesion load or T1 hypointense lesion load during 2.8 years of follow-up (CIS + RRMS). Conclusion: These results do not support a strong role of 8,12-iso-iPF2alpha-VI in the prediction of disease progression in MS.
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Bauer, Jochen, Anne Ripperger, Stefan Frantz, Süleyman Ergün, Edzard Schwedhelm, and Ralf A. Benndorf. "Pathophysiology of isoprostanes in the cardiovascular system: implications of isoprostane-mediated thromboxane A2receptor activation." British Journal of Pharmacology 171, no. 13 (June 10, 2014): 3115–31. http://dx.doi.org/10.1111/bph.12677.
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Härtlová, H., R. Rajmon, A. Dörflerová, L. Zita, D. Řehák, J. Rosmus, M. Šindelář, and P. Klabanová. "Effect of Dietary Supplementation with Vitamin E and Selenium in Thoroughbred Horses on the Concentration of F2-isoprostanes in the Blood Plasma as a Marker of Lipid Peroxidation." Acta Veterinaria Brno 77, no. 3 (2008): 335–40. http://dx.doi.org/10.2754/avb200877030335.
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The objective of this study was to assess the effect of vitamin E and selenium (Se) supplementation on the plasma levels of F2-isoprostanes as a marker of oxidative stress in horses in their training period. Twelve healthy 3-year-old English thoroughbred horses were divided into two groups: control (n = 6) and experimental (n = 6). Feeding rations were adapted to a moderate workload. The horses of the experimental group received supplements of DL-α-tocopheryl acetate E (2 250 mg/day/horse) and of sodium selenite (0.5 mg/day/horse). The plasma concentrations of both antioxidants and F2-isoprostanes were monitored on days 0, 44 and 70. After 70 days of supplementation, the concentrations of selenium in the experimental group were significantly higher (P < 0.05) compared to the beginning of the experiment (mean ± SE: 135.81 ± 10.19 μg l -1 vs. 98.70 ± 10.88 μg l -1), as well as to the control group (day 0: 101.78 ± 11.06 μg l -1, day 70: 108.18 ± 7.77 μg l -1). In the horses of the experimental group, plasma α-tocopherol levels significantly increased from the 44th day of supplementation compared to the beginning of the study as well to the control group (5.23 ± 0.52 mg l -1 vs. 2.45 ± 0.25 mg l -1 or 3.46 ± 0.34 mg l -1, respectively). The plasma concentration of F2-isoprostanes tended to be lower in the experimental group at the end than at the beginning of monitoring (156.8 ± 12.89 pg l -1 vs. 170.3 ± 60.8 pg l -1), although the control group showed the opposite trend (181.2 ± 15.67 pg l -1 vs. 137.0 ± 47.05 pg l -1). Nevertheless, none of these differences were significant because of the large variability of the individual values. It can be stated that supplementation of the diet used with selenium and vitamin E caused a non-significant decrease of F2-isoprostane concentration in the blood plasma only, and a significant increase of plasma concentrations of these antioxidants. The variation of isoprostane levels probably reflected rather the individual responses of the horses' organisms to the training workload.
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Belli, R., P. Amerio, L. Brunetti, G. Orlando, P. Toto, G. Proietto, M. Vacca, and A. Tulli. "Elevated 8-Isoprostane Levels in Basal Cell Carcinoma and in Uva Irradiated Skin." International Journal of Immunopathology and Pharmacology 18, no. 3 (July 2005): 497–502. http://dx.doi.org/10.1177/039463200501800309.
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Isoprostanes are prostaglandin isomers produced from the peroxidation of polyunsaturated fatty acids from the cellular membrane. They have been used as a specific index of cellular lipoperoxidation and as an indirect measure of oxidative stress. However, these molecules also present several biological activities. An oxidative environment measured as the presence of other indirect measurements of reactive oxygen species lipoperoxidation has recently been described in basal cell carcinoma, the most frequent type of non-melanoma skin cancer. This study aims to measure the levels of 8-isoprostaglandin F2α, an isoprostane widely studied in other models as a by-product of ROS-induced lipid peroxidation, in basal cell carcinoma and in UVA irradiated healthy skin. We found that 8-iso-PGF2α is present in higher levels in BCC specimens compared to healthy non sun-exposed skin, confirming previous studies on the production of lipoperoxidation in this tumor. Moreover, we demonstrated that topical pre-treatment with a compound containing vitamin E is capable of reducing 8-iso-PGF2α formation in UV irradiated skin suggesting a role for isoprostanes in UV induced inflammation and eventually carcinogenesis and confirming the function of vitamin E as an antioxidant in this model.
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Brooks, Joshua D., Ginger L. Milne, Huiyong Yin, Stephanie C. Sanchez, Ned A. Porter, and Jason D. Morrow. "Formation of Highly Reactive Cyclopentenone Isoprostane Compounds (A3/J3-Isoprostanes) in Vivo from Eicosapentaenoic Acid." Journal of Biological Chemistry 283, no. 18 (February 10, 2008): 12043–55. http://dx.doi.org/10.1074/jbc.m800122200.
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Ortiz-Ruiz, Clara M., Elizabeth Sanabria, Melissa C. Manriquez, Rodney J. Bolterman, Luis A. Juncos, and Juan C. Romero. "The Role of Endothelin and Oxidative Stress in the Slow Pressor Responses to Angiotensin II (ANG II)." Hypertension 36, suppl_1 (October 2000): 685. http://dx.doi.org/10.1161/hyp.36.suppl_1.685-d.
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44 Chronic infusion of subpressor doses of Ang II causes blood pressure to increase progressively over several days. The mechanisms underlying this response are unknown but may involve Ang II-induced generation of additional vasoconstrictor processes. In this study, we tested whether endothelin and/or oxidative stress are implicated in the slow pressor responses to Ang II. We infused either vehicle (group 1; n=6) or Ang II (group 2; n=5) intravenously at 5 ng/kg/min via osmotic pumps for 15 days into Sprague Dawley rats. In addition to the Ang II infusion, groups 3 and 4 (n=6 each) received 30 mg/kg/day of either losartan (an angiotensin AT 1 receptor blocker) or bosentan (a blocker of both endothelin receptors, ET A and ET B ) in their drinking water. We measured systolic blood pressure (SBP) during the infusion, and the levels of circulating Ang II and isoprostanes (a marker of oxidative stress) at the conclusion of the experiments. Rats infused with vehicle had no change in SBP (from 138±13 to 138±2 mmHg) and normal levels of Ang II (34.5±9 pg/ml) and isoprostanes (111±10 pg/ml). Ang II infusion increased SBP from 133±10 to 158±8 mmHg, as well as circulating levels of Ang II (144±65 pg/ml) and isoprostanes (156±19 pg/ml). Losartan treatment abolished Ang II induced increases in SBP (SBP went from 137±5 to 120±4 mmHg), and isoprostanes (115±15 pg/ml), without altering Ang II levels (101±30 pg/ml). Bosentan also blocked Ang II-induced increases in SBP (from 135±4 to 139±3) but did not alter the increased isoprostane levels (146±14 pg/ml). Surprisingly, bosentan blunted the increase in Ang II levels (51±10 pg/ml). In conclusion, low dose Ang II-induced increases in SBP and oxidant stress depend on the AT 1 receptor. Endothelin receptor blockade also reduces SBP, but it does so independently of reducing oxidative stress (as measured by isoprostanes).
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Gerald, Carresse L., Chakia J. McClendon, Rohit S. Ranabhat, Jenora T. Waterman, Lauren L. Kloc, Dawn R. Conklin, Ke’Yona T. Barton, Janak R. Khatiwada, and Leonard L. Williams. "Sorrel Extract Reduces Oxidant Production in Airway Epithelial Cells Exposed to Swine Barn Dust Extract In Vitro." Mediators of Inflammation 2019 (August 1, 2019): 1–11. http://dx.doi.org/10.1155/2019/7420468.
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Exposure to hog barn organic dust contributes to occupational lung diseases, which are mediated by inflammatory and oxidative stress pathways. Isoprostanes—a family of eicosanoids produced by oxidation of phospholipids by oxygen radicals—are biomarkers of pulmonary oxidative stress. Importantly, 8-isoprostane has been implicated as a key biomarker and mediator of oxidative stress because it is a potent pulmonary vasoconstrictor. Antioxidants found in fruits and vegetables hold promise for preventing or reducing effects of oxidative stress-related diseases including chronic bronchitis and chronic obstructive pulmonary disease (COPD). Here, we investigated 8-isoP and oxidant production by organic dust-exposed airway epithelial cells and the inhibitory effects of an extract from calyces of the sorrel plant, Hibiscus sabdariffa, on oxidant-producing pathways. Confluent cultures of normal human tracheobronchial epithelial cells were pretreated or not with 1% sorrel extract prior to 5% dust extract (DE) exposure. Following DE treatments, live cells, cell-free supernatants, or cell extracts were evaluated for the presence of 8-isoprostane, superoxide, hydrogen peroxide, nitric oxide, hydroxyl radical, peroxynitrite, and catalase activity to evaluate sorrel’s inhibitory effect on oxidative stress. The well-known radical scavenging antioxidant, N-acetyl cysteine (NAC), was used for comparisons with sorrel. DE exposure augmented the production of all radicals measured including 8-isoprostane (p value < 0.001), which could be inhibited by NAC or sorrel. Among reactive oxygen and nitrogen species generated in response to DE exposure, sorrel had no effect on H2O2 production and NAC had no significant effect on NO⋅ production. The observations reported here suggest a possible role for sorrel in preventing 8-isoprostane and oxidant-mediated stress responses in bronchial epithelial cells exposed to hog barn dust. These findings suggest a potential role for oxidative stress pathways in mediating occupational lung diseases and antioxidants within sorrel and NAC in reducing dust-mediated oxidative stress within the airways of exposed workers.
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Liu, Caiqiong, Tracy Tazzeo, and Luke J. Janssen. "Isoprostane-induced airway hyperresponsiveness is dependent on internal Ca2+ handling and Rho/ROCK signaling." American Journal of Physiology-Lung Cellular and Molecular Physiology 291, no. 6 (December 2006): L1177—L1184. http://dx.doi.org/10.1152/ajplung.00142.2006.
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We previously reported the ability of isoprostanes to induce airway hyperresponsiveness (AHR). In this study, we examined the signaling mechanisms underlying that phenomenon with the standard muscle bath technique. Responses to a threshold concentration of carbachol (CCh, 3 × 10−9 M) were significantly augmented by pretreatment for 20 min with 8-isoprostaglandin E2 (15-E2t-IsoP, 10−6 M): this AHR was obliterated in tissues pretreated with the selective Rho kinase (ROCK) inhibitor Y-27632 added 20 min before isoprostane, but not by cyclopiazonic acid (CPA). Increasing the CCh concentration to 3 × 10−8 M (still considerably less than the half-maximally effective concentration of CCh) evoked larger contractions that were also augmented significantly by 15-E2t-IsoP: this AHR was completely abolished in tissues pretreated with CPA as well as those pretreated with Y-27632. We noted, however, that Y-27632 and CPA profoundly effect baseline tone and the cholinergic response per se, which confounds the interpretation of the data summarized above. We therefore modified the protocol by using combinations of CCh and blocker (CPA, Y-27632, or nifedipine) that were equieffective. In this way, we found that AHR could not be demonstrated under conditions in which Rho/ROCK signaling or Ca2+ release was abolished (by Y-27632 and CPA, respectively). Likewise, other autacoids that act through G protein-coupled receptors via Rho/ROCK and Ca2+ release (serotonin, histamine) mimicked this effect of isoprostane, whereas bradykinin did not. We conclude that isoprostane-induced AHR is mediated in part through an action on Rho/ROCK signaling. This novel finding may contribute to a better understanding of the mechanisms underlying AHR and asthma.
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Härtlová, Helena, Radko Rajmon, Iva Krontorádová, Jiří Mamica, Lukáš Zita, Petra Klabanová, and Antonín Černocký. "Semen quality, lipid peroxidation, and seminal plasma antioxidant status in horses with different intensities of physical exercise." Acta Veterinaria Brno 82, no. 1 (2013): 31–35. http://dx.doi.org/10.2754/avb201382010031.
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The aim of this study was to compare markers of semen quality, sperm membrane damage, and the seminal plasma antioxidant activity in warmblood stallions with and without sport workload stress. Four stallions were used for breeding only (control) and four both for breeding and competition in jumping. Semen samples were collected at 14-day intervals (from June to August) from each stallion (5 ejaculates per stallion). Immediately after sperm collection, a conventional examination of the ejaculate was processed. Catalytic activities of enzymes aspartate aminotransferase, alanin aminotransferase, glutathione peroxidase, superoxide dismutase and indicator of lipoperoxidation - F2α isoprostanes were measured in samples of seminal plasma. Contrary to basic semen quality indicators, the values of seminal plasma pH, aspartate aminotransferase and alanin aminotransferase were significantly (P < 0.05) impaired in the physically stressed stallions. Also, the level of F2α isoprostanes and the activity of superoxide dismutase were significantly (P < 0.05) increased by stress. The antioxidant activities of superoxide dismutase and glutathion peroxidase increased during the monitored period and reflected changes in F2α isoprostane concentration. We can conclude that even the conventional basic sperm indicators stay within the reference ranges of the biochemical indicators of seminal plasma such as pH or AST/ALT activity may be negatively influenced by sport workload stress. Increased concentrations of F2α isoprostanes indicate that lipoperoxidation can be a mechanism of cell membrane destabilization, which is counteracted by an increase of antioxidant enzyme activities. This is the first report of oxidative stress symptoms in normospermic equine semen in relation to stallion sport workload.
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Alkazemi, Dalal, Robert L. Jackson, Hing Man Chan, and Stan Kubow. "Increased F3-Isoprostanes in the Canadian Inuit Population Could Be Cardioprotective by Limiting F2-Isoprostane Production." Journal of Clinical Endocrinology & Metabolism 101, no. 9 (September 2016): 3264–71. http://dx.doi.org/10.1210/jc.2015-4096.
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Ting, Harold J., and Fadi T. Khasawneh. "Platelet function and Isoprostane biology. Should Isoprostanes be the newest member of the Orphan-ligand family?" Journal of Biomedical Science 17, no. 1 (2010): 24. http://dx.doi.org/10.1186/1423-0127-17-24.
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Catalli, Adriana, and Luke J. Janssen. "Augmentation of bovine airway smooth muscle responsiveness to carbachol, KCl, and histamine by the isoprostane 8-iso-PGE2." American Journal of Physiology-Lung Cellular and Molecular Physiology 287, no. 5 (November 2004): L1035—L1041. http://dx.doi.org/10.1152/ajplung.00138.2004.
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Isoprostanes are generated during periods of oxidative stress, which characterize diseases such as asthma and cystic fibrosis. They also elicit functional responses and may therefore contribute to the pathology of these diseases. We set out to examine the effects of isoprostanes on airway responsiveness to cholinergic stimulation. Muscle bath techniques were employed using isolated bovine tracheal smooth muscle. 8-Isoprostaglandin E2 (8-iso-PGE2) increased tone directly on its own, although the magnitude of this response, even at the highest concentration tested, was only a fraction of that evoked by KCl or carbachol. More importantly, though, pretreatment of the tissues with 8-iso-PGE2 (10 μM) markedly augmented responses to submaximal and even subthreshold concentrations of KCl, carbachol, or histamine, whereas maximal responses to these agents were unaffected by the isoprostane. The augmentative effect on cholinergic responsiveness was mimicked by PGE2 (0.1 μM) and by the FP agonists PGF2 (0.1 μM) and fluprostenol (0.1 μM), but not by the EP3 agonist sulprostone (0.1 μM) or the TP agonist U-46619 (0.1 μM). Antagonists of EP1 receptors (AH-6809 and SC-19920, 10 μM) and TP receptors (ICI-192605, 1 μM) had no effect on 8-iso-PGE2-induced augmentation of cholinergic responsiveness. We conclude that 8-iso-PGE2 induces nonspecific airway smooth muscle hyperresponsiveness through a non-TP non-EP prostanoid receptor.
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Helmersson, Johanna, Johan Ärnlöv, Anders Larsson, and Samar Basu. "Low dietary intake of β-carotene, α-tocopherol and ascorbic acid is associated with increased inflammatory and oxidative stress status in a Swedish cohort." British Journal of Nutrition 101, no. 12 (December 15, 2008): 1775–82. http://dx.doi.org/10.1017/s0007114508147377.
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Fruit and vegetable consumption has been associated with a reduced risk of several diseases including CVD. A part of these effects seen could be linked to anti-inflammatory and antioxidative effects, although this has not been thoroughly investigated. The present study was designed to investigate the effects of the dietary intake of β-carotene, α-tocopherol and ascorbic acid on in vivo biomarkers of inflammation (PGF2α, high-sensitive C-reactive protein (hsCRP) and IL-6 formation) and oxidative stress (F2-isoprostane formation), the two important factors associated with accelerated atherosclerosis. The dietary intake of 704 participants in the Uppsala Longitudinal Study of Adult Men (ULSAM) at age 70 years was registered and inflammatory and oxidative stress biomarkers were quantified 7 years later. The registered dietary intakes of ascorbic acid and α-tocopherol were negatively associated linearly and in quartiles with both PGF2α, hsCRP, IL-6 and F2-isoprostanes, where ascorbic acid intake generally was more strongly associated. Dietary intake of β-carotene was only significantly negatively associated with F2-isoprostanes. In conclusion, the present study is the first to suggest that the intake of food rich in antioxidants is associated with reduced cyclo-oxygenase- and cytokine-mediated inflammation and oxidative stress at 7 years of follow-up. These associations could be linked to the beneficial effects of fruit and vegetables observed on CVD.
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Dai, Qi, Yu-Tang Gao, Xiao-Ou Shu, Gong Yang, Ginger Milne, Qiuyin Cai, Wanqing Wen, et al. "Oxidative Stress, Obesity, and Breast Cancer Risk: Results From the Shanghai Women's Health Study." Journal of Clinical Oncology 27, no. 15 (May 20, 2009): 2482–88. http://dx.doi.org/10.1200/jco.2008.19.7970.
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Purpose Increased reactive oxygen species may exhaust the antioxidant capability of human defense systems, leading to oxidative stress and cancer development. Urinary F2-isoprostanes, secondary end products of lipid peroxidation, are more accurate markers of oxidative stress than other available biomarkers. No prospective study has investigated whether levels of 15-F2t-isoprostane (15-F2t-IsoP) and its metabolite 2,3-dinor-5,6-dihydro-15-F2t-IsoP (15-F2t-IsoPM) are related to breast cancer risk. Patients and Methods We conducted a nested case-control study within the Shanghai Women's Health Study, a population-based cohort study of 74,942 Chinese women between 40 and 70 years of age. Prediagnostic urinary 15-F2t-IsoP and 15-F2t-IsoPM were measured by gas chromatography mass spectrometry for 436 breast cancer cases and 852 individually matched controls. Results Urinary excretion of isoprostanes was not significantly different between cases and controls. However, among overweight women, levels of isoprostanes were positively associated with breast cancer risk, which became stronger with increasing body mass index (BMI). Among women with a BMI ≥ 29, the odds ratio (OR) increased to 10.27 (95% CI, 2.41 to 43.80) for the highest compared with the lowest tertile of 15-F2t-IsoPM (P for trend = .003; P for interaction = .0004). In contrast, 15-F2t-IsoP and 15-F2t-IsoPM were inversely associated with breast cancer risk among nonoverweight women. Among women with a BMI ≤ 23, breast cancer risk was reduced with increasing 15-F2t-IsoP levels in a dose-response manner (P for trend = .006), with an OR of 0.46 (95% CI, 0.26 to 0.80) for the highest tertile versus the lowest (P for interaction = .006). Conclusion Our results suggest that the role of oxidative stress in breast cancer development may depend on adiposity.
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Kayamba, Violet, and Paul Kelly. "Estimated 24-hour urinary sodium excretion as a risk factor for oxidative stress in Zambian adults: A cross-sectional study." PLOS ONE 15, no. 11 (November 12, 2020): e0242144. http://dx.doi.org/10.1371/journal.pone.0242144.
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Introduction Persistent oxidative stress predisposes to various non-communicable diseases (NCDs), whose occurrence is increasing in sub-Saharan Africa. The aim of this study was to evaluate the link between markers of oxidative stress and some risk factors for NCDs in a Zambian cohort. Methods We assessed oxidative stress by measuring 8-isoprostane (lipid oxidative stress) and 8-hydroxydeoxyguanosine (DNA oxidative stress). In addition, we measured mycotoxins (aflatoxin M1 and ochratoxin A), salt intake estimated from 24-hour sodium excretion calculated using the Tanaka and Kawaski formulae, and 1-hydroxypyrene (a metabolite of polycyclic aromatic hydrocarbons). Data on lifestyle risk factors were collected using questionnaires. Results Included were 244 participants; 128 (52%) were female and the median age was 48 years (IQR 39–58). The median level of 8-isoprostane was 0.13 ng/mg creatinine (IQR 0.08–0.23) while that of 8-hydroxydeoxyguanosine (8-OHdG) was 4 ng/mg creatinine (IQR 2–10). The median 24-hour sodium excretion was 21 g (IQR 16–25 g), with none being less than the 5 g recommended by WHO. Unadjusted urinary levels of 8-isoprostane were moderately correlated with 1-hydroxypyrene (Spearman r = 0.30, p<0.001) and estimated 24-hour urine sodium (Spearman r = 0.38, p<0.001). Urinary levels of 8-OHdG were not correlated with 1-hydroxypyrene, estimated 24-hour urine sodium, aflatoxin M1 or ochratoxin A (all p-values >0.05). Using logistic regression, adjusted and unadjusted 8-isoprostanes levels were associated with 1-hydroxypyrene (p = 0.02 and p = 0.001 respectively) and estimated 24-hour urine sodium method (p = 0.003 and p<0.001 respectively). However, only unadjusted 8-OHdG was associated with 1-hydroxypyrene (p = 0.03) and age (p = 0.007). Conclusions Estimated 24-hour urinary sodium is high among Zambians and it is associated with lipid but not DNA oxidative stress. High exposure to polycyclic aromatic hydrocarbons is also associated with oxidative stress.
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Bi, Wenzhao, Geeng-Fu Jang, Lei Zhang, John W. Crabb, James Laird, Mikhail Linetsky, and Robert G. Salomon. "The Adductomics of Isolevuglandins: Oxidation of IsoLG Pyrrole Intermediates Generates Pyrrole–Pyrrole Crosslinks and Lactams." High-Throughput 8, no. 2 (May 10, 2019): 12. http://dx.doi.org/10.3390/ht8020012.
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Isoprostane endoperoxides generated by free radical-induced oxidation of arachidonates, and prostaglandin endoperoxides generated through enzymatic cyclooxygenation of arachidonate, rearrange nonenzymatically to isoprostanes and a family of stereo and structurally isomeric γ-ketoaldehyde seco-isoprostanes, collectively known as isolevuglandins (isoLGs). IsoLGs are stealthy toxins, and free isoLGs are not detected in vivo. Rather, covalent adducts are found to incorporate lysyl ε-amino residues of proteins or ethanolamino residues of phospholipids. In vitro studies have revealed that adduction occurs within seconds and is uniquely prone to cause protein–protein crosslinks. IsoLGs accelerate the formation of the type of amyloid beta oligomers that have been associated with neurotoxicity. Under air, isoLG-derived pyrroles generated initially are readily oxidized to lactams and undergo rapid oxidative coupling to pyrrole–pyrrole crosslinked dimers, and to more highly oxygenated derivatives of those dimers. We have now found that pure isoLG-derived pyrroles, which can be generated under anoxic conditions, do not readily undergo oxidative coupling. Rather, dimer formation only occurs after an induction period by an autocatalytic oxidative coupling. The stable free-radical TEMPO abolishes the induction period, catalyzing rapid oxidative coupling. The amine N-oxide TMAO is similarly effective in catalyzing the oxidative coupling of isoLG pyrroles. N-acetylcysteine abolishes the generation of pyrrole–pyrrole crosslinks. Instead pyrrole-cysteine adducts are produced. Two unified single-electron transfer mechanisms are proposed for crosslink and pyrrole-cysteine adduct formation from isoLG-pyrroles, as well as for their oxidation to lactams and hydroxylactams.
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Haram, Kjell, Jan Helge Mortensen, Ole Myking, Everett F. Magann, and John C. Morrison. "The Role of Oxidative Stress, Adhesion Molecules and Antioxidants in Preeclampsia." Current Hypertension Reviews 15, no. 2 (May 29, 2019): 105–12. http://dx.doi.org/10.2174/1573402115666190119163942.
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Oxidative stress is a consequence of reduction in the antioxidant capacity and excessive production of reactive oxygen and nitrogen species (ROS). Oxidative agents, which are overproduced due to ischemic-reperfusion injury in the placenta, may overwhelm the normal antioxidant activity. This imbalance is a key feature in the pathogenesis of preeclampsia. A decrease in glutathione peroxidase (GPX) activity is associated with the synthesis of vasoconstrictive eicosanoids such as F2-isoprostanes and thromboxane, which are known to be upregulated in preeclampsia. Biochemical markers of lipid peroxidation, such as malondialdehyde and F2-isoprostane in the placenta, are also increased. Adhesion molecules participate in the pathophysiology of preeclampsia by contributing to a reduced invasion by the trophoblast and increased vascular endothelial damage. Superoxide dismutase (SOD), catalase (CAT) and GPX play important roles counteracting oxidative stress. Other antioxidant factors participate in the etiology of preeclampsia. Levels of antioxidants such as Lycopene, Coenzyme 10, as well as some vitamins, are reduced in preeclamptic gestations.
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Shizuka, Manami, Thomas O. Schrader, and Marc L. Snapper. "Synthesis of Isoprostanyl Phosphatidylcholine and Isoprostanyl Phosphatidylethanolamine." Journal of Organic Chemistry 71, no. 4 (February 2006): 1330–34. http://dx.doi.org/10.1021/jo0518553.
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Mahmoudi, Michael, Juan Guillermo Gormaz, Marcia Erazo, Michael Howard, Cristian Baeza, Martin Feelisch, Nick Curzen, et al. "Early Oxidative Stress Response in Patients with Severe Aortic Stenosis Undergoing Transcatheter and Surgical Aortic Valve Replacement: A Transatlantic Study." Oxidative Medicine and Cellular Longevity 2019 (November 13, 2019): 1–8. http://dx.doi.org/10.1155/2019/6217837.
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Myocardial ischemia/reperfusion-related oxidative stress as a result of cardiopulmonary bypass is thought to contribute to the adverse clinical outcomes following surgical aortic valve replacement (SAVR). Although the acute response following this procedure has been well characterized, much less is known about the nature and extent of oxidative stress induced by the transcatheter aortic valve replacement (TAVR) procedure. We therefore sought to examine and directly compare the oxidative stress response in patients undergoing TAVR and SAVR. A total of 60 patients were prospectively enrolled in this exploratory study, 38 patients undergoing TAVR and 22 patients SAVR. Reduced and oxidized glutathione (GSH, GSSG) in red blood cells as well as the ferric-reducing ability of plasma (FRAP) and plasma concentrations of 8-isoprostanes were measured at baseline (S1), during early reperfusion (S2), and 6-8 hours (S3) following aortic valve replacement (AVR). TAVR and SAVR were successful in all patients. Patients undergoing TAVR were older (79.3±9.5 vs. 74.2±4.1 years; P<0.01) and had a higher mean STS risk score (6.6±4.8 vs. 3.2±3.0; P<0.001) than patients undergoing SAVR. At baseline, FRAP and 8-isoprostane plasma concentrations were similar between the two groups, but erythrocytic GSH concentrations were significantly lower in the TAVR group. After AVR, FRAP was markedly higher in the TAVR group, whereas 8-isoprostane concentrations were significantly elevated in the SAVR group. In conclusion, TAVR appears not to cause acute oxidative stress and may even improve the antioxidant capacity in the extracellular compartment.
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Marijančević, Domagoj, Nada Vrkić, Igor Jukić, and Daniel Bok. "Alterations in redox homeostasis following repeated sprint training." Kinesiology 52, no. 1 (2020): 19–29. http://dx.doi.org/10.26582/k.52.1.3.
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This study examined the effects of a 6-week repeated sprint training on redox-based homeostasis and their association with muscle damage. Fifteen male physical education students (aged 20.0±1.0 years; body weight 77.7±6.0 kg; height 181.0±4.4 cm; %body fat 8.7±3.0 %), familiar with intermittent activities, volunteered to participate in the study. Experimental training program consisted of 2-3 sets of 6-10 straight-line or shuttle 20-m repeated sprints with departures every 25 seconds and a 2-minute inter-set passive recovery. The training intervention lasted six weeks during which 18 training sessions were performed. The levels were measured of the following: 15-F2t-isoprostanes in plasma and 24-hour urine; superoxide dismutase, glutathione peroxidase and glutathione reductase in erythrocytes; uric acid and creatine kinase in serum after the first and the penultimate training session. The level of muscle damage following the repeated sprint exercise was not significantly altered (402 to 496 U/L; p=.151) and had no significant associations with the changes in markers depicting redox-homeostasis. A significant increase in plasma 15-F2t-isoprostanes (0.32 to 0.56 ng/mL; p=.026), and a subsequent decrease in glutathione reductase (7.7 to 3.4 U/g Hb; p<.001) were observed. Urinary 15-F2t-isoprostane levels were 25% greater at post-training, although this increase did not reach statistical significance. These results indicate that repeated sprint training stimulates the equilibrium in redox homeostasis developing antioxidant protection to the constantly increasing training load.
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Schuster, Daniel P., James K. Kozlowski, Tim McCarthy, Jason Morrow, and Alan Stephenson. "Effect of endotoxin on oleic acid lung injury does not depend on priming." Journal of Applied Physiology 91, no. 5 (November 1, 2001): 2047–54. http://dx.doi.org/10.1152/jappl.2001.91.5.2047.
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Recent studies have demonstrated significant synergistic physiological and biochemical effects between low-dose endotoxin (Etx) administration and oleic acid (OA)-induced canine lung injury. To evaluate whether this interaction depends on Etx priming of some key cell population, we compared the effects of giving low-dose Etx both after as well as before inducing lung injury with OA. In addition to hemodynamic and blood-gas measurements, positron emission tomographic imaging was used to measure edema accumulation and intrapulmonary blood flow distribution. Biochemical measurements of the stable metabolites of prostacyclin and thromboxane were obtained as well as measurements of isoprostanes and reactive sulfhydryls as evidence for possible concomitant oxidant production. We found that the physiological and biochemical effects of low-dose Etx developed 30–45 min after its administration, regardless of whether Etx was administered before or after OA. No increase in either isoprostane or reactive sulfhydryl production after Etx and/or OA was detected. These data suggest that the synergistic effect of low-dose Etx and OA-induced lung injury is not due to a priming effect of Etx.
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GARCÍA-ESTAÑ, Joaquín, M. Clara ORTIZ, and Samuel S. LEE. "Nitric oxide and renal and cardiac dysfunction in cirrhosis." Clinical Science 102, no. 2 (January 14, 2002): 213–22. http://dx.doi.org/10.1042/cs1020213.
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Nitric oxide (NO) has diverse physiological and pathophysiological effects. The roles of NO in the renal and cardiac dysfunction found in cirrhosis are reviewed. In the kidneys of experimental animals with cirrhosis, several lines of evidence speak in favour of an enhanced production of NO, through the activation of both endothelial constitutive and inducible isoforms of NO synthase. In contrast with the situation in normal animals, inhibition of NO synthesis in rats with cirrhosis improves sodium and water excretion via blood pressure-dependent and -independent mechanisms, which indicates that the renal sodium and water retention of cirrhosis is related to an excess of NO production. The deleterious effect of excessive NO on the kidney may be mediated by peroxynitrite, a potent oxidant that is readily formed whenever superoxide anions and the ·NO radical are produced together. The peroxidation of arachidonic acid by peroxynitrite leads to the formation of F2a-isoprostanes, which are powerful renal vasoconstrictors. F2a-isoprostane levels are correlated with the severity of liver injury during cirrhosis. However, whether peroxynitrite or F2a-isoprostanes are the elusive mediator of the NO-induced renal alterations in cirrhosis remains to be firmly established. NO is also involved in cardiac contractility, probably in the normal heart as well as in disease conditions such as non-cirrhotic and cirrhotic cardiomyopathy. In the latter state, evidence suggests that inducible NO synthase attenuates ventricular contractility, mediated by cGMP. Another gas that transduces its signal through cGMP, carbon monoxide, is also likely to play a role in cirrhotic cardiomyopathy, but the nature of the interaction between NO and carbon monoxide in this syndrome remains unclear.
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Imran, Imran, Konrad Koch, Henrik Schöfer, Helene Lau, and Jochen Klein. "Effects of Three Anti-Seizure Drugs on Cholinergic and Metabolic Activity in Experimental Status Epilepticus." Journal of Pharmacy & Pharmaceutical Sciences 22 (July 26, 2019): 340–51. http://dx.doi.org/10.18433/jpps30439.
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Purpose. Status epilepticus (SE) is characterized by recurrent seizure activity and can be drug-resistant. Knowledge of neuronal and metabolic activity of the brain during SE may be helpful to improve medical care. We here report the effects of three anti-seizure drugs on changes of acetylcholine energy metabolites and oxidative stress during SE. Methods. We used the lithium-pilocarpine model in rats to induce SE and in vivo-microdialysis to monitor cholinergic and metabolic activity in the hippocampus. We measured extracellular concentrations of acetylcholine, glucose, lactate, pyruvate, glycerol and isoprostanes before and during SE, and after acute treatment with pregabalin, valproic acid, and levetiracteam. Results. Upon onset of SE, acetylcholine (ACh) release increased six- to eightfold. Glucose was increased only transiently by 30% but lactate levels rose four-fold, and extracellular concentrations of glycerol ten-fold. Isoprostanes are markers of oxidative stress and increased more than 20-fold. Two hours after pilocarpine adminstration, rats were treated with pregabalin (100 mg/kg), levetiracetam (200 mg/kg) or valproic acid (400 mg/kg) by i.p. injection. All three drugs stopped seizure activity in a delayed fashion, but at the doses indicated, only animals that received levetiracetam reached consciousness. All drugs reduced ACh release within 60-120 minutes. Lactate/pyruvate ratios, glycerol and isoprostanne levels were also reduced significantly after drug administration. Conclusions. Hippocampal ACh release closely follows seizure activity in SE and is attenuated when SE subsides. Pregabalin, valproic acid and levetiracetam all terminate seizures in the rat SE model and attenuate cholinergic and metabolic changes within two hours.
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Roberts, L. Jackson, and Ginger L. Milne. "Isoprostanes." Journal of Lipid Research 50, Supplement (October 28, 2008): S219—S223. http://dx.doi.org/10.1194/jlr.r800037-jlr200.
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ROBERTS, L. JACKSON, and JASON D. MORROW. "Isoprostanes." Annals of the New York Academy of Sciences 744, no. 1 Cellular Gene (November 1994): 237–42. http://dx.doi.org/10.1111/j.1749-6632.1994.tb52741.x.
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