Relevant bibliographies by topics / Isoprostany

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Academic literature on the topic 'Isoprostany'

Author: Grafiati
Published: 4 June 2021
Last updated: 1 February 2022

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Journal articles on the topic "Isoprostany"

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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 &lt;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 &lt;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 &lt;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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Dissertations / Theses on the topic "Isoprostany"

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Silva, Graziela Biude. "Estado nutricional relativo ao zinco de pacientes com artrite reumatoide e sua relação com o estresse oxidativo e o polimorfismo Arg213Gli no gene da superóxido dimutase 3." Universidade de São Paulo, 2013. http://www.teses.usp.br/teses/disponiveis/9/9132/tde-27022014-103035/.

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A artrite reumatoide (AR) é uma doença auto-imune de etiologia desconhecida caracterizada por uma inflamação poliarticular simétrica da membrana sinovial que acomete com maior frequência as articulações das mãos, punhos e pés. Estudos mostram que há um aumento do estresse oxidativo nestes pacientes e este fato pode ser atribuído à diminuição da ingestão de substâncias antioxidantes refletindo no aumento da produção de espécies reativas de oxigênio (ERO). Além disso, a presença de polimorfismos em enzimas antioxidantes como o Arg213Gli no gene da enzima superóxido dismutase 3 podem influenciar neste dano oxidativo. Portanto, o estudo teve como objetivo avaliar o estado nutricional relativo ao zinco de pacientes com artrite reumatoide e sua relação com o estresse oxidativo e o polimorfismo Arg213Gli no gene da SOD3. Foram selecionadas 59 mulheres diagnosticadas com AR (59,9±18,3 anos) atendidas no Setor de Reumatologia do Hospital São Paulo/Universidade Federal de São Paulo, que fizeram parte do grupo caso, e 56 mulheres saudáveis (35,5±9,9 anos) recrutadas no campus da Universidade de São Paulo, que fizeram parte do grupo controle. A coleta de sangue venoso foi destinada para avaliação das concentrações plasmática e eritrocitária de zinco, da atividade das enzimas glutationa peroxidase (GPx) e superóxido dismutase (SOD), e do polimorfismo Arg213Gli. A urina de 24 horas foi coletada para as análises de zinco, creatinina e 8-isoprostanos. A avaliação do consumo dietético de zinco foi feita por meio de três recordatórios alimentares de 24 horas. A análise estatística foi feita no software SPSS 14.0 por meio de testes de comparações de médias e correlações selecionados de acordo com a distribuição da normalidade e considerando p significativo menor que 5%. As concentrações plasmáticas de zinco foram significativamente menores para o grupo caso quando comparadas ao grupo controle (53,4±9,8 µg/dL e 58,2±10,1 µg/dL, respectivamente; p=0,011). Com relação às concentrações de zinco eritrocitário e urinário não houve diferença significativa entre os grupos (p=0,219 e p=0,695, respectivamente). O percentual de inadequação do consumo de zinco foi de 98,9% para o grupo caso e 58% para o grupo controle. A atividade da SOD foi significativamente menor no grupo caso (1333,8 ±420,8 U/gHb) do que no grupo controle (1755,0 ±525,5 U/gHb) (p<0,001), assim como a atividade da GPx (38,2 ±17,0 U/gHb e 52,6 ±14,4 U/gHB, respectivamente) (p<0,001). As concentrações de 8-isoprostanos não diferiram entre os grupos caso e controle, (133,8 ±175,4 ng/mmol de creatinina e 139,3 ± 52,7 ng/mmol de creatinina; p=0,836, respectivamente). Em relação à genotipagem do SNP Arg213Gli não foi encontrado nenhuma participante com o genótipo homozigoto (Gli/Gli) para o polimorfismo. No grupo caso, apenas uma participante apresentou o genótipo heterozigoto (Arg/Gli). Os resultados apresentados indicam que as pacientes com AR estão deficientes em zinco e apresentam um aumento do estresse oxidativo, sugerindo a necessidade de uma suplementação deste mineral.
Rheumatoid arthritis (RA) is an autoimmune disease of unknown etiology characterized by a symmetrical polyarticular inflammation of synovial membrane that affects most often the joints of the hands, wrists and feet. Studies show that there is an increase of oxidative stress in these patients and this fact can be attributed to decreased intake of antioxidants reflecting in the increased production of reactive oxygen species (ROS). Furthermore, the presence of polymorphisms in antioxidant enzymes such as Arg213Gli in the superoxide dismutase gene may influence this oxidative damage. Thus, the study aimed to evaluate the nutritional status of zinc in patients with rheumatoid arthritis and its relation to oxidative stress and the polymorphism Arg213Gli in SOD3 gene. We selected 59 women diagnosed with RA ( 59.9 ± 18.3 years) which make clinical monitoring at the Hospital São Paulo/Federal University of São Paulo, who were part of the case group, and 56 healthy women ( 35.5 ± 9 , 9 years) recruited on the campus of the University of São Paulo, who were part of the control group. The venous blood collection was destined to evaluate plasma and erythrocyte zinc, activity of glutathione peroxidase (GPx) and superoxide dismutase (SOD), and the polymorphism Arg213Gli. The 24-hour urine was collected for the analyzes of zinc, creatinine and 8- isoprostane. The assessment of dietary intake of zinc was performed by three 24-hour dietary recall. Statistical analysis was performed with SPSS 14.0 by testing of mean comparisons and correlations selected according to the distribution of normality and considering significant p less than 5 %. The plasma zinc concentrations were significantly lower in the case group compared to the control group (53.4 ± 9.8 µg/dL and 58.2 ± 10.1µg/dL, respectively, p= 0.011). In relation to the concentrations of erythrocyte and urinary zinc, no significant difference was observed between groups (p= 0.219 and p=0.695, respectively). The percentage of inadequate zinc intake was 98.9% for the case group and 58% for the control group . The SOD activity was significantly lower in the case group (1333.8 ± 420.8 U/gHb) than in the control group (1755.0 ± 525.5 U/gHb) (p < 0.001), as well as the activity of GPx (38.2 ± 17.0 U/gHb and 52.6 ± 14.4 U/gHb, respectively) (p< 0.001). The 8-isoprostane concentrations did not differ between case and control groups (133.8 ± 175.4 ng/mmol creatinine and 139.3 ± 52.7 ng/mmol creatinine, p= 0.836, respectively). Regarding Arg213Gli SNP genotyping was not found any participant with the homozygous genotype (Gly/Gly) for the polymorphism. In case group, only one participant had the heterozygous genotype (Arg/Gly). The presented results indicate that RA patients are deficient in zinc and have an increased oxidative stress, suggesting the need for a supplementation of this mineral.
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Čumová, Martina. "Využití hmotnostní spektrometrie ke stanovení markerů oxidativního stresu a mykotoxinů." Doctoral thesis, Vysoké učení technické v Brně. Fakulta chemická, 2015. http://www.nusl.cz/ntk/nusl-233402.

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The first topic presented in the dissertation thesis is determination of isoprostanes as markers of oxidative stress and other compounds affected by presence of oxidative stress. Isoprostanes iPF2-III, iPF2-VI, iPF2-VI, astaxanthin and polyunsaturated fatty acids (PUFA), especially arachidonic acid (AA) were monitored in Atlantic salmon eggs (Salmo salar). Methods for the determination of these compounds have been developed and optimized using chromatographic separation coupled to conventional or mass spectrometric detection. Freshly laid eggs, eyed embryos and non-viable eggs were used to test a general hypothesis that egg viability can be affected by susceptibility to oxidative stress, either through the specific fatty acid concentration and/or the antioxidant capacity of the eggs. Levels of isoprostanes and arachidonic acid (AA) were significantly higher in non-viable eggs than in control (eyed embryos) as well as relative abundance of PUFA. While no difference of isoprostanes was found between freshly laid and control those from the Atlantic stock except iPF2-VI which was observed under the LOQ in the control. Higher levels of PUFA and AA in comparison with the control were observed in the freshly laid eggs. However, the only statistically significant difference was observed in the amount of astaxanthin. Different levels of PUFA and astaxanthin may be related to their biochemical consumption during the development of eggs. This work evaluated potential effect on the viability of eggs Salmo salar due to the presence of oxidative stress. The monitoring of mycotoxins in food and feed was the subject of the second topic. Mycotoxins are secondary metabolites produced by fungi. They are ubiquitous undesirable natural contaminants that are toxic for humans and animals. Today are known more than 500 mycotoxins. However, only few of them are regulated by the European Union. The European Food Safety Authority (EFSA) was asked by the European Commission to provide a scientific opinion on other mycotoxins for which statutory limits could be developed. In this study is proposed simultaneous screening allowing fast, reliable and sensitive approach, identification and quantification of 17 mycotoxins in food and feed sample. The method includes both mycotoxins regulated by the EU and selected mycotoxins required by the EFSA (aflatoxins, deoxynivalenol, nivalenol, zearalenone, fumonisin, ochratoxin A, T-2 toxin, HT-2 toxin, enniatins and beauvericin). Analytes are isolated by the modified QuEChERS method. For separation and target mycotoxins detection, ultra-performance liquid chromatography coupled to tandem mass spectrometry (UPLC –MS/MS) was employed. The method also allows determination of ergot alkaloids (ergocornine, ergosine, ergocryptine, ergocristine and their respective epimers). The developed method was used either for monitoring mycotoxins and ergot alkaloids in feed and raw materials and barley and malt prepared from it.
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Martinez, Bermudez Ana Katherine. "Isoprostanes in brain endothelial cell death." Thesis, McGill University, 1998. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=21605.

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Oxygen free radicals have been implicated in several diseases including ischemic stroke, and myocardial infarction. They can trigger chain reactions like peroxidation of membrane phospholipids, leading to osmotic imbalance and cell death. Isoprostanes are stable products of lipid peroxidation that have a constrictor effect on the vasculature and bronchii. As isoprostanes are abundantly generated in tissues under oxidant stress, we have hypothesized that they could be related to endothelial dysfunction observed during ischemia/reperfasion by affecting endothelial cell survival. The effects of 8-iso-PGE2 and 8-iso-PGF2alpha, two abundantly produced isoprostanes, were studied on porcine endothelial cultures and isolated brain microvessels. Cell survival was evaluated by MTT reduction, double staining with DNA-binding fluorochromes and in situ DNA fragmentation labeling,
8-Iso-PGF2alpha (1--10 nM) induced 20--25% cell death in endothelial cultures after 24 h coincident with similar increase in the number of cells that become permeable to PI. On the contrary, 8-iso-PGE 2 did not affect endothelial cell survival. Approximately 9% of the cells suffered apoptosis. This percentage remained unchanged regardless the treatment. Several observations indicate a role for thromboxane A2 to mediate 8-iso-PGF2alpha-induced death: (1) the levels of thromboxane A2 increased dramatically in endothelial cultures after 8-iso-PGF2alpha-treatment; (2) inhibitors of thromboxane synthase, CGS12970 and U6355A and Ibuprofen, a non-selective inhibitor of cyclooxygenases, reverted the effect of the isoprostane; (3) analogs of thromboxane A2 U46619 and IBOP, reproduce the effect of 8-iso-PGF 2alpha after 24 h. 8-Iso-PGF2alpha also decreased endothelial viability on isolated brain microvessels. These results suggest, that 8-iso-PGF2alpha, might be a direct contributor to ischemia/reperfusion injury.
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Martinez, Bermudez Ana Katherine. "Isoprostanes in brain endothelial cell death." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape9/PQDD_0025/MQ50832.pdf.

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Henry, Olivier. "Synthèses totales de métabolites de la 15-F2t-Isoprostane." Montpellier 2, 2002. http://www.theses.fr/2002MON20009.

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Freitas, Betânia de Jesus e. Silva de Almendra 1962. "Possíveis marcadores de estresse oxidativo para câncer de pele não melanoma : efeito da suplementação de vitamina C, E e mineral zinco em indivíduos que tiveram câncer de pele não melanoma." [s.n.], 2014. http://repositorio.unicamp.br/jspui/handle/REPOSIP/312979.

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Abstract:
Orientador: Patrícia Moriel
Tese (doutorado) - Universidade Estadual de Campinas, Faculdade de Ciências Médicas
Made available in DSpace on 2018-08-26T00:37:20Z (GMT). No. of bitstreams: 1 Freitas_BetaniadeJesuseSilvadeAlmendra_D.pdf: 2657931 bytes, checksum: d4646bbc60ccc13e11ca7d806b4f75dc (MD5) Previous issue date: 2014
Resumo: Estudos acerca da influência do estresse oxidativo sobre o equilíbrio cutâneo, sobretudo por seus efeitos devastadores sobre a integridade da pele, são essenciais para a proposição de estratégias de intervenção preventivas para o desenvolvimento do câncer de pele. O objetivo do estudo foi comparar o estresse oxidativo de indivíduos que tiveram e não tiveram câncer de pele não melanoma e avaliar o efeito da suplementação combinada de vitaminas C, E e mineral Zinco no estresse oxidativo de indivíduos que apresentaram a doença. O estudo foi dividido em duas fases: a fase 1 foi um estudo transversal com controles, cuja população foi constituída por pessoas saudáveis (n = 24) e o grupo caso constituído por indivíduos que apresentaram câncer de pele não melanoma já submetidas a tratamento cirúrgico (n = 60). E a fase 2, um ensaio clínico randomizado e duplo cego, no qual os pacientes do grupo caso foram randomizados em dois subgrupos: grupo placebo (n = 34) e grupo suplementado (n = 26) com 50 mg de vitamina C, 60 mg de vitamina E e 40 mg de Zinco durante 8 semanas. As amostras de sangue dos sujeitos foram obtidas no período basal e após intervenção para a avaliação dos biomarcadores de estresse oxidativo (F2-isoprostano, nitrito, substâncias reativas ao ácido tiobarbitúrico (TBARS) e capacidade antioxidante total). O consumo alimentar habitual e o estado nutricional dos sujeitos foram avaliados. Para identificação dos fatores associados ao câncer de pele foi utilizada a análise de regressão logística univariada e multivariada. O nível de significância adotado para este estudo foi de 5%. A maioria dos pacientes estudados foram do sexo feminino com idade superior a 50 anos. Os pacientes do grupo caso apresentaram mais elevadas concentrações séricas dos biomarcadores de estresse oxidativo, sendo que as concentrações de F2-isoprostano estavam significativamente mais elevadas em comparação com os controles. Após suplementação não houve diferença estatística entre os grupos placebo e suplementado em relação aos marcadores de estresse oxidativo. A idade e o F2-isoprostano podem ser marcadores de risco para o câncer de pele não melanoma, a cada ano a mais para o fator idade aumenta em 12% a chance de câncer e cada unidade a mais na medida do marcador aumenta em 4% a chance de câncer. Os resultados mostraram prevalência de sobrepeso no grupo controle com diferença estatística significativa em relação ao grupo caso. As concentrações dietéticas dos minerais antioxidantes zinco, cobre e selênio do grupo caso foram estatisticamente inferiores em relação aos controles e não houve diferença estatística nas concentrações dietéticas dos nutrientes antioxidantes entre os grupos suplementado e placebo. Este estudo sugere que pessoas diagnosticadas com câncer de pele não melanoma e que no momento da realização da pesquisa não mais apresentavam a doença, mostravam elevado estresse oxidativo, quando comparadas a pessoas saudáveis. A suplementação de antioxidantes pelo período de tempo realizado no trabalho não provocou redução significativa nas concentrações dos marcadores de estresse oxidativo dos pacientes. O estudo ainda sugere que o marcador de estresse oxidativo F2-isoprostano pode ser utilizado como um fator de risco para o desenvolvimento do câncer de pele não melanoma
Abstract: Studies investigating the influence of oxidative stress on skin homeostasis, especially for its devastating effects on skin integrity, are essential for the development of preventive intervention strategies for skin cancer. The goal of this study was to compare the concentrations of oxidative stress biomarkers in blood between individuals with and without non-melanoma skin cancer and evaluate the effect of combined supplementation with vitamins C, E, and the mineral zinc on oxidative stress in skin-cancer patients. The study was divided into two stages: stage 1 was cross-sectional study with controls, whose population consisted of healthy individuals (n = 24) and the case group included individuals who had non-melanoma skin cancer undergoing surgery (n = 60). And the second phase a randomized, double blind clinical trial where patients in the case group were randomized into two subgroups: placebo (n =34) and a supplemented group (n = 26) who received 50 mg of vitamin C, 60 mg of vitamin E, and 40 mg of zinc for 8 wk. Blood samples were taken from the subjects before and after intervention to evaluate levels of oxidative stress biomarkers (F2-isoprostane, nitrite, thiobarbituric acid reactive substances (TBARS) and total antioxidant capacity. The usual food consumption and nutritional state of the subjects were also evaluated. Multivariate and univariate logistics regression analysis were used to identify factors associated with the development of skin cancer. The level of significance adopted for this study was 5%. The majority of participants were women over the age of 50. The patients in the case group had higher serum concentrations of oxidative stress biomarkers, and the levels of F2-isoprostane were significantly higher than the controls. After antioxidant supplementation there was no statistical difference in the markers of oxidative stress among the placebo and supplemented groups. Age and F2-isoprostane may be effective biomarkers for estimating the risk of non-melanoma skin cancer development. Moreover, the risk of cancer increases with age at a rate of 12% per year, while an increase in concentration of these biomarker in blood increases the risk of cancer by 4%. These results showed a prevalence of excess weight in the control group with significant statistical difference from the case group. The dietary intake of the mineral antioxidants zinc, copper, and selenium of the case group were significantly lower than the control group, and there was no statistical difference in the dietary intake of the antioxidant nutrients among the supplemented and placebo groups. This study suggests that people diagnosed with non-melanoma skin cancer and those in remission at the time of the study, exhibited higher concentration oxidative stress than healthy individuals. The antioxidant supplementation by period the work performed did not cause significant reduction in serum concentrations of oxidative stress biomarkers of the patients. The results suggest that the concentration of the oxidative stress biomarker, F2-isoprostane, may serve as risk factor for non-melanoma skin cancer development
Doutorado
Ciencias Biomedicas
Doutora em Ciências Médicas
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Pinot, Edith. "Synthèse totale des quatre diastéréoisomères de la 15-E2t-isoprostane." Montpellier 2, 2008. http://www.theses.fr/2008MON20014.

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Dinca, Emanuela [Verfasser], and Thomas [Akademischer Betreuer] Lindel. "Oxidative Reactions of Enolates and Their Application to Total Syntheses of 15-F2t-Isoprostane and Potential Secondary Metabolites of 15-E2-Isoprostane / Emanuela Dinca ; Betreuer: Thomas Lindel." Braunschweig : Technische Universität Braunschweig, 2013. http://d-nb.info/1175821438/34.

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Greaves, Kim. "Influence of Isoprostane F2[subscript a] -III on reflow after myocardial infarction." Thesis, King's College London (University of London), 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.439447.

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Clarke, Deborah Lee. "The role of prostanoids and isoprostanes in airway inflammation." Thesis, Imperial College London, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.406342.

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Books on the topic "Isoprostany"

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Gopaul, Nitin Kumar. Analysis of F2-isoprostanes as markers of lipid peroxidation. Oxford: Oxford Brookes University, 1997.

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Book chapters on the topic "Isoprostany"

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Arndt, T. "Isoprostane." In Springer Reference Medizin, 1296–97. Berlin, Heidelberg: Springer Berlin Heidelberg, 2019. http://dx.doi.org/10.1007/978-3-662-48986-4_1638.

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Arndt, T. "Isoprostane." In Lexikon der Medizinischen Laboratoriumsdiagnostik, 1–2. Berlin, Heidelberg: Springer Berlin Heidelberg, 2017. http://dx.doi.org/10.1007/978-3-662-49054-9_1638-1.

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Jackson Roberts, L., Cynthia J. Brame, Yan Chen, Jason D. Morrow, and Robert G. Salomon. "Formation of Reactive Products of the Isoprostane Pathway: Isolevuglandins and Cyclopentenone Isoprostanes." In Advances in Experimental Medicine and Biology, 335–41. Boston, MA: Springer US, 1999. http://dx.doi.org/10.1007/978-1-4615-4793-8_49.

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Roberts, L. Jackson, Yan Chen, Olivier Boutaud, Sean S. Davies, Jason D. Morrow, John A. Oates, and Cynthia Brame. "Reactive Products of the Isoprostane Pathway: Isoketals and Cyclopentenone A2/J2-Isoprostanes." In Advances in Prostaglandin and Leukotriene Research, 191–95. Dordrecht: Springer Netherlands, 2001. http://dx.doi.org/10.1007/978-94-015-9721-0_37.

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Callewaert, Denis M., and Charles Sloan. "Enzyme Immunoassay of Isoprostanes." In Methods in Molecular Biology, 435–49. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60327-029-8_26.

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Ciabattoni, G., P. Patrignani, M. R. Panara, A. Greco, F. Cipollone, G. Davi, G. Di Minno, A. Coppola, and C. Patrono. "Studies of Isoprostane Biosynthesis in Man." In Eicosanoids, 111–15. Boston, MA: Springer US, 1996. http://dx.doi.org/10.1007/978-1-4899-0200-9_11.

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Loeffler, Christane, Ingeborg Thoma, Markus Krischke, and Martin J. Mueller. "The Dinor Isoprostane Pathway in Plants." In Advances in Experimental Medicine and Biology, 217–20. Boston, MA: Springer US, 2003. http://dx.doi.org/10.1007/978-1-4419-9194-2_47.

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McNamara, Peter, John A. Lawson, Joshua Rokach, and Garret A. FitzGerald. "Isoprostane Activation of the Nuclear Hormone Receptor Ppar." In Advances in Experimental Medicine and Biology, 351–55. Boston, MA: Springer US, 2002. http://dx.doi.org/10.1007/978-1-4615-0193-0_54.

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Montuschi, Paolo, Peter J. Barnes, and Giovanni Ciabattoni. "Measurement of 8-Isoprostane in Exhaled Breath Condensate." In Methods in Molecular Biology, 73–84. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60761-411-1_5.

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Sinzinger, Helmut, Anthony Oguogho, and Heidemarie Pilz. "Increased Isoprostanes in Children of Smoking Parents." In Advances in Experimental Medicine and Biology, 213–15. Boston, MA: Springer US, 2003. http://dx.doi.org/10.1007/978-1-4419-9194-2_46.

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Conference papers on the topic "Isoprostany"

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Reitman, Aaron J., Rachel Chapman, Danielle Markus, David Bliss, Jessica L. Wisnowski, Thomas Coates, Philippe Friedlich, Ginger Milne, and John Wood. "Plasma f2-isoprostane Levels in Neonatal Extracorporeal Membrane Oxygenation." In Selection of Abstracts From NCE 2016. American Academy of Pediatrics, 2018. http://dx.doi.org/10.1542/peds.141.1_meetingabstract.577.

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Kummarapurugu, Apparao B., Ziqiang Guan, Bernard M. Fischer, Ginger L. Milne, Erin Potts-Kant, W. M. Foster, and Judith A. Voynow. "NQO1 Regulates Cellular Redox Status And Ozone-Induced Isoprostane Generation." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a6848.

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Reitman, Aaron J., Rachel Chapman, Danielle Markus, David Bliss, Ginger Milne, Thomas Coates, Philippe Friedlich, John Wood, and Jessica L. Wisnowski. "Plasma f2-isoprostane Levels in Neonatal Extra Corporeal Membrane Oxygenation*." In Selection of Abstracts From NCE 2016. American Academy of Pediatrics, 2018. http://dx.doi.org/10.1542/peds.141.1_meetingabstract.317.

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Liu, M., G. Lu, C. Li, J. Su, R. Jiang, and R. Zhang. "8-Isoprostane F2α in Chronic Thromboembolic Pulmonary Hypertension: A Novel Biomarker?" In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a6047.

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Hadley, Graham, Susan Stephenson, Madhuri Penugonda, and Anne M. Fitzpatrick. "Plasma 8-Isoprostane Levels As A Biomarker Of Asthma Severity In Children." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a5480.

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Chamitava, Liliya, Lucia Cazzoletti, Marcello Ferrari, Paolo Degan, Andrea Pasini, Anna Fratta-Pasini, Morena Nicolis, et al. "White blood cells, FeNO, glutathione, 8-oxodG and 8-isoprostane in respiratory diseases." In ERS International Congress 2016 abstracts. European Respiratory Society, 2016. http://dx.doi.org/10.1183/13993003.congress-2016.pa4239.

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Turnbull, Christopher, Ioannis Akoumianakis, Malcolm Kohler, Charalambos Antoniades, and John Stradling. "Overnight urinary isoprostane levels during CPAP withdrawal as a marker of oxidative stress." In ERS International Congress 2016 abstracts. European Respiratory Society, 2016. http://dx.doi.org/10.1183/13993003.congress-2016.pa2071.

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Jackson, Robert M., Chhavi Gupta, Carol Ramos, and Orlando Gomez. "Exercise Decreases Plasma Antioxidants And Increases Urinary Isoprostanes In IPF Patients." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a5323.

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Zhang, Rui, You-Fei Fan, Dong Liu, Ping Yuan, Wen-Hui Wu, Zeenat Safdar, and Zhi-Cheng Jing. "8-Isoprostane F2± In Idiopathic Pulmonary Arterial Hypertension: A Novel Biomarker Of Poor Prognosis." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a3816.

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Türk, Murat, Oğuz Köktürk, Zeynep Işıkdoğan, and Canan Demirtaş. "Urinary biomarkers for obstructive sleep apnea syndrome: Lipocalin type prostaglandin-D synthase and F2-isoprostane." In ERS International Congress 2018 abstracts. European Respiratory Society, 2018. http://dx.doi.org/10.1183/13993003.congress-2018.pa2535.

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