898 resultados para Oxidative stress in epilepsy


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This study aimed to assess the effect of percutaneous transthoracic lung biopsy on the oxidative metabolism of sheep by measuring the oxidative stress markers of superoxide dismutase (SOD), total glutathione (GSH-t), peroxidase (GSH-Px) and thiobarbituric acid reactive substances (TBARS) in the red cells of these animals. Blood samples were collected from 20 clinically healthy sheep prior to, and 30 min after, percutaneous transthoracic lung biopsy. After biopsy, there was a significant decrease (p < 0.05) in SOD and GSH-Px activity, with no significant change (p ≥ 0.05) in GSH-t and TBARS concentrations. These results showed that percutaneous transthoracic lung biopsy did not significantly affect the oxidative metabolism of sheep 30 min after the procedure, which may be used widely in this species without causing serious tissue damage. © 2012. The Authors.

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Among the numerous coadjuvant therapies that could influence the incidence and progression of diabetic complications, antioxidants and flavonoids are currently being tested in clinical trials. We investigated the effect of quercetin on biochemical parameters in streptozotocin-induced (60 mg/kg body mass, by intraperitoneal injection) diabetic rats. A total of 32 female Wistar rats were distributed among 4 groups as follows: control (G1); control treated with quercetin (G2); diabetic (G3); and diabetic treated with quercetin (G4). Quercetin administered to pregnant diabetic rats controlled dyslipidemia and improved lipid profiles in diabetes mellitus, regulated oxidative stress by reducing the generation of lipid hydroperoxides, and increased the activity of the antioxidant enzyme glutathione peroxidase.

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Background: Citrus flavonoids, such as hesperidin, have shown therapeutic properties that improve hyperglycemia and insulin resistance, and decrease blood serum lipids and inflammation. The current investigation studied the effects of hesperidin supplementation associated with continuous and interval swimming on the biochemical parameters (glucose, cholesterol and triglycerides), and oxidative stress markers (TBARS and DPPH) in rats.Methods: The animals (n = 60) were randomly divided in six groups: negative (C) and positive control (CH) for hesperidin supplementation, and continuous or interval swimming without (CS and IS) or with hesperidin supplementation (CSH and ISH). Hesperidin was given by gavage for four weeks (100 mg/kg body mass) before the exercise. Continuous swimming was performed for 50 min with loads from 5% to 8 % of body weight from the first to fourth week, while interval swimming training was performed for 50 min in sessions of 1 min of swimming followed by 2 min of resting, carrying loads from 10% to 15, 20 and 25% from the first to fourth week. At the end of the experiment, blood serum samples were draw to perform analysis of glucose, total cholesterol, HDL-C and triglycerides. Oxidative biomarkers were evaluated by lipid peroxidation (TBARS) and antioxidant capacity assay (DPPH) of the blood serum.Results: There was a continuous decline of serum glucose from C (100%) > CH (97%) > CS (94%) > CSH (91%, p < .05), IS (87%, p < .05) > ISH (80%, p < .05), showing a combined beneficial effect of hesperidin and swimming. Also, continuous or intermittent swimming with hesperidin supplementation lowered total cholesterol (-16%, p < .05), LDL-C (-50%, p < 0.05) and triglycerides (-19%, p < 0.05), and increased HDL-C (48%, p < .05). Furthermore, hesperidin enhanced the antioxidant capacity on the continuous swimming group (183%, p < .05) and lowered the lipid peroxidation on the interval swimming group (-45%, p < .05).Conclusions: Hesperidin supplementation per se, or in combination with swimming exercise protocols, improved the biochemical profile and antioxidant biomarkers evidencing that the use of flavanones may enhance the health benefits promoted by exercise. © 2013 de Oliveira et al.; licensee BioMed Central Ltd.

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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

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Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)

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To evaluate the effect of the oxidative stress on human dental pulp cells (HDPCs) promoted by toxic concentrations of hydrogen peroxide (H2O2) on its odontoblastic differentiation capability through time. Methods HDPCs were exposed to two different concentrations of H2O2 (0.1 and 0.3 μg/ml) for 30 min. Thereafter, cell viability (MTT assay) and oxidative stress generation (H2DCFDA fluorescence assay) were immediately evaluated. Data were compared with those for alkaline phosphatase (ALP) activity (thymolphthalein assay) and mineralized nodule deposition (alizarin red) by HDPCs cultured for 7 days in osteogenic medium. Results A significant reduction in cell viability and oxidative stress generation occurred in the H2O2-treated cells when compared with negative controls (no treatment), in a concentration-dependent fashion. Seven days after H2O2 treatment, the cells showed significant reduction in ALP activity compared with negative control and no mineralized nodule deposition. Conclusion Both concentrations of H2O2 were toxic to the cells, causing intense cellular oxidative stress, which interfered with the odontogenic differentiation capability of the HDPCs. Clinical significance The intense oxidative stress on HDPCs mediated by H2O2 at toxic concentrations promotes intense reduction on odontoblastic differentiation capability in a 7-day evaluation period, which may alter the initial pulp healing capability in the in vivo situation.

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Abdominal adiposity has been linked to metabolic abnormalities, including dyslipidemia, oxidative stress, and low-grade inflammation. To test the hypothesis that consumption of 100% orange juice (OJ) would improve metabolic, oxidative, and inflammatory biomarkers and cytokine levels in normal and overweight subjects with increased waist circumference. Subjects were divided into two groups in accordance with their body mass index: normal and overweight. Both groups of individuals consumed 750 mL of OJ daily for 8 weeks. Body composition (weight, height, percentage of fat mass, and waist circumference); metabolic biomarkers (total cholesterol, low-density lipoprotein-cholesterol [LDL-C], high-density lipoprotein-cholesterol [HDL-C], triglycerides, glucose, insulin, HOMA-IR, and glycated hemoglobin); oxidative biomarkers (malondialdehyde and DPPH(•)); inflammatory biomarkers (high-sensitivity C-reactive protein [hsCRP]); cytokines (IL-4, IL-10, IL-12, TNF-α, and IFN-γ); and diet were evaluated before and after consumption of OJ for 8 weeks. The major findings of this study were: 1) no alteration in body composition in either group; 2) improvement of the lipid profile, evidenced by a reduction in total cholesterol and LDL-C; 3) a potential stimulation of the immune response due to increase in IL-12; 4) anti-inflammatory effect as a result of a marked reduction in hsCRP; and 5) antioxidant action by the enhancement of total antioxidant capacity and the reduction of lipid peroxidation, in both normal and overweight subjects. OJ consumption has a positive effect on important biomarkers of health status in normal and overweight subjects, thereby supporting evidence that OJ acts as functional food and could be consumed as part of a healthy diet to prevent metabolic and chronic diseases.

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Background: Over 6 million people die annually in the world because of cancer. Several groups are focused on studying cancer chemoprevention approaches. Resveratrol, a polyphenol, at high dosages, has been reported as antitumor and chemopreventive. However, it has a dose-dependent effect on cell death, even on some cancer cells. Objectives: Our aim was to investigate this dose-dependent effect on human bladder carcinoma ECV304 cells during oxidative stress condition. Methods: For this purpose. ECV304 cells incubated with different Resveratrol concentrations were analyzed as for their metabolic rate, membrane permeability, DNA fragmentation, anti/proapoptotic protein levels and phosphatidylserine exposure after oxidative stress. Results: Resveratrol induced cell death at high concentrations (>20 mu M), but not at low ones (0.1-20 mu M). Pretreatment with 2.5 mu M protected the cells from oxidative damage, whereas 50 mu M intensified the cell death and significantly increased Bad/Bcl-2 ratio (proapoptotic/antiapoptotic proteins). Resveratrol was able to modulate NO and PGE(2) secretion and performed an anti-adhesion activity of neutrophils on PMA-activated ECV304 cells. Conclusions: Resveratrol at high doses induces cell death of ECV304 cells whereas low doses induce protection. Modulation of Bcl-2 protein induced by Resveratrol could be mediating this effect. This information about the role of Resveratrol on cancer alerts us about its dose-dependent effects and could lead the design of future chemoprevention strategies. Published by Elsevier Ireland Ltd.

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Malaria associated-acute kidney injury (AKI) is associated with 45% of mortality in adult patients hospitalized with severe form of the disease. However, the causes that lead to a framework of malaria-associated AKI are still poorly characterized. Some clinical studies speculate that oxidative stress products, a characteristic of Plasmodium infection, as well as proinflammatory response induced by the parasite are involved in its pathophysiology. Therefore, we aimed to investigate the development of malaria-associated AKI during infection by P. berghei ANKA, with special attention to the role played by the inflammatory response and the involvement of oxidative stress. For that, we took advantage of an experimental model of severe malaria that showed significant changes in the renal pathophysiology to investigate the role of malaria infection in the renal microvascular permeability and tissue injury. Therefore, BALB/c mice were infected with P. berghei ANKA. To assess renal function, creatinine, blood urea nitrogen, and ratio of proteinuria and creatininuria were evaluated. The products of oxidative stress, as well as cytokine profile were quantified in plasma and renal tissue. The change of renal microvascular permeability, tissue hypoxia and cellular apoptosis were also evaluated. Parasite infection resulted in renal dysfunction. Furthermore, we observed increased expression of adhesion molecule, proinflammatory cytokines and products of oxidative stress, associated with a decrease mRNA expression of HO-1 in kidney tissue of infected mice. The measurement of lipoprotein oxidizability also showed a significant increase in plasma of infected animals. Together, our findings support the idea that products of oxidative stress, as well as the immune response against the parasite are crucial to changes in kidney architecture and microvascular endothelial permeability of BALB/c mice infected with P. berghei ANKA.

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Bucioli, SA, de Abreu, LC, Valenti, VE, and Vannucchi, H. Carnitine supplementation effects on nonenzymatic antioxidants in young rats submitted to exhaustive exercise stress. J Strength Cond Res 26(6): 1695-1700, 2012-Previous studies have demonstrated that exercise stress increases oxidative stress in rats. However, antioxidant supplement therapy effects on reactive oxygen substances are conflicting. We evaluated the effects of carnitine on renal nonenzymatic antioxidants in young rats submitted to exhaustive exercise stress. Wistar rats were divided into 3 groups: (a) control group (not submitted to exercise stress), (b) exercise stress group, and (c) exercise stress and carnitine group. The rats from group 3 were treated with gavage administration of 1 ml of carnitine (5 mg.kg(-1)) for 7 consecutive days. The animals from groups 2 and 3 were submitted to a bout of swimming exhaustive exercise stress. Kidney samples were analyzed for reactive substances to thiobarbituric acid by malondialdehyde (MDA), reduced glutathione (GSH), and vitamin-E levels. Carnitine treatment attenuated MDA increase caused by exercise stress (1:0.16 +/- 0.02 vs. 2:0.34 +/- 0.07 vs. 3:0.1 +/- 0.01 mmmol per milligram of protein; p < 0.0001). It also increased the renal levels of GSH (1:23 +/- 4 vs. 2:23 +/- 2 vs. 3:58 +/- 9 mu mol per gram of protein; p, 0.0001); however, it did not change renal vitamin E (1:24 +/- 5 vs. 2:27 +/- 1 vs. 3:28 +/- 5 mu M per gram of tissue; p < 0.001). In conclusion, carnitine improved oxidative stress and partially improved the nonenzymatic antioxidant activity in young rats submitted to exhaustive exercise stress.

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Possa SS, Charafeddine HT, Righetti RF, da Silva PA, Almeida-Reis R, Saraiva-Romanholo BM, Perini A, Prado CM, Leick-Maldonado EA, Martins MA, Tiberio ID. Rho-kinase inhibition attenuates airway responsiveness, inflammation, matrix remodeling, and oxidative stress activation induced by chronic inflammation. Am J Physiol Lung Cell Mol Physiol 303: L939-L952, 2012. First published September 21, 2012; doi:10.1152/ajplung.00034.2012.-Several studies have demonstrated the importance of Rho-kinase in the modulation of smooth muscle contraction, airway hyperresponsiveness, and inflammation. However, the effects of repeated treatment with a specific inhibitor of this pathway have not been previously investigated. We evaluated the effects of repeated treatment with Y-27632, a highly selective Rho-kinase inhibitor, on airway hyperresponsiveness, oxidative stress activation, extracellular matrix remodeling, eosinophilic inflammation, and cytokine expression in an animal model of chronic airway inflammation. Guinea pigs were subjected to seven ovalbumin or saline exposures. The treatment with Y-27632 (1 mM) started at the fifth inhalation. Seventy-two hours after the seventh inhalation, the animals' pulmonary mechanics were evaluated, and exhaled nitric oxide (E-NO) was collected. The lungs were removed, and histological analysis was performed using morphometry. Treatment with Y-27632 in sensitized animals reduced E-NO concentrations, maximal responses of resistance, elastance of the respiratory system, eosinophil counts, collagen and elastic fiber contents, the numbers of cells positive for IL-2, IL-4, IL-5, IL-13, inducible nitric oxide synthase, matrix metalloproteinase-9, tissue inhibitor of metalloproteinase-1, transforming growth factor-beta, NF-kappa B, IFN-gamma, and 8-iso-prostaglandin F2 alpha contents compared with the untreated group (P < 0.05). We observed positive correlations among the functional responses and inflammation, remodeling, and oxidative stress pathway activation markers evaluated. In conclusion, Rho-kinase pathway activation contributes to the potentiation of the hyperresponsiveness, inflammation, the extracellular matrix remodeling process, and oxidative stress activation. These results suggest that Rho-kinase inhibitors represent potential pharmacological tools for the control of asthma.

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We investigated the role of aminoguanidine and benfotiamine on the inhibition of reactive oxygen species (ROS) generation in macrophages induced by advanced glycated albumin (AGE-albumin) and its relationship with cell cholesterol homeostasis, emphasizing the expression of the ATP binding cassette transporter A-1 (ABCA-1). AGE-albumin was made by incubating fatty acid-free albumin with 10 mM glycolaldehyde. ROS production and ABCA-1 protein level were determined by flow cytometry in J774 macrophages treated along time with control (C) or AGE-albumin alone or in the presence of aminoguanidine or benfotiamine. Mitochondrial function was evaluated by oxygraphy. Compared to C-albumin, AGE-albumin increased ROS production in macrophages, which was ascribed to the activities of NADPH oxidase and of the mitochondrial system. Mitochondrial respiratory chain activity was reduced in cells incubated with AGE-albumin. ROS generation along time was associated with the reduction in macrophage ABCA-1 protein level. Aminoguanidine prevented ROS elevation and restored the ABCA-1 content in macrophages; on the other hand, benfotiamine that promoted a lesser reduction in ROS generation was not able to restore ABCA-1 levels. Inhibition of oxidative stress induced by AGE-albumin prevents disturbances in reverse cholesterol transport by curbing the reduction of ABCA-1 elicited by advanced glycation in macrophages and therefore may contribute to the prevention of atherosclerosis in diabetes mellitus.

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Background: Mechanisms linking behavioral stress and inflammation are poorly understood, mainly in distal lung tissue. Objective: We have investigated whether the forced swim stress (FS) could modulate lung tissue mechanics, iNOS, cytokines, oxidative stress activation, eosinophilic recruitment, and remodeling in guinea pigs (GP) with chronic pulmonary inflammation. Methods: The GP were exposed to ovalbumin or saline aerosols (2x/wk/4wks, OVA, and SAL). Twenty-four hours after the 4th inhalation, the GP were submitted to the FS protocol (5x/wk/2wks, SAL-S, and OVA-S). Seventy-two hours after the 7th inhalation, lung strips were cut and tissue resistance (Rt) and elastance (Et) were obtained (at baseline and after OVA and Ach challenge). Strips were submitted to histopathological evaluation. Results: The adrenals' weight, the serum cortisol, and the catecholamines were measured. There was an increase in IL-2, IL-5, IL-13, IFN-gamma, iNOS, 8-iso-PGF2 alpha, and in %Rt and %Et after Ach challenge in the SAL-S group compared to the SAL one. The OVA-S group has had an increase in %Rt and %Et after the OVA challenge, in %Et after the Ach and in IL-4, 8-iso-PGF2 alpha, and actin compared to the OVA. Adrenal weight and cortisol serum were increased in stressed animals compared to nonstressed ones, and the catecholamines were unaltered. Conclusion & clinical relevance: Repeated stress has increased distal lung constriction, which was associated with an increase of actin, IL-4, and 8-iso-PGF2 alpha levels. Stress has also induced an activation of iNOS, cytokines, and oxidative stress pathways.

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Purpose: To assess the relationship between the presence of pets in homes of epilepsy patients and the occurrence of sudden unexpected death in epilepsy (SUDEP). Methods: Parents or relatives of SUDEP patients collected over a ten-year period (2000-2009) in a large epilepsy unit were asked if the patient lived together with any domestic pet at the time of death or not. Patients who did not experience SUDEP served as controls. Results and conclusions: Eleven out of the 1092 included patients (1%) experienced SUDEP, all with refractory symptomatic epilepsy, but none of them had pets in their homes at the time of death. In contrast, the frequency of pet-ownership in the control group (n = 1081) was 61%. According to previous studies there are some indications that human health is directly related to companionship with animals in a way that domestic animals prevent illness and facilitate recovery of patients. Companion animals can buffer reactivity against acute stress, diminish stress perception and improve physical health. These factors may reduce cardiac arrhythmias and seizure frequency, factors related to SUDEP. Companion animals may have a positive effect on well-being, thus irnproving epilepsy outcome. (c) 2012 British Epilepsy Association. Published by Elsevier Ltd. All rights reserved.

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Non-mechanised sugarcane harvesting preceded by burning exposes workers and the people of neighbouring towns to high concentrations of pollutants. This study was aimed to evaluate the respiratory symptoms, lung function and oxidative stress markers in sugarcane workers and the residents of Mendonca, an agricultural town in Brazil, during the non-harvesting and harvesting periods and to assess the population and individual exposures to fine particulate matter (PM2.5). Sugarcane workers and healthy volunteers were evaluated with two respiratory symptom questionnaires, spirometry, urinary 1-hydroxypyrene levels, and the measurement of antioxidant enzymes and plasma malonaldehyde during the non-harvesting and harvesting periods. The environmental assessment was determined from PM2.5 concentration. PM2.5 level increased from 8 mu g/m(3) during the non-harvesting period to 23.5 mu g/m(3) in the town and 61 mu g/m(3) on the plantations during the harvesting period. Wheezing, coughing, sneezing, and breathlessness increased significantly in both groups during the harvesting period, but more markedly in workers. A decrease in lung function and antioxidant enzyme activity was observed in both populations during harvesting; this decrease was greater among the sugarcane workers. The urinary 1-hydroxypyrene levels only increased in the sugarcane workers during the harvesting period. The malonaldehyde levels were elevated in both groups, with a higher increase observed in the workers. This research demonstrates the exposure of sugarcane workers and the inhabitants of a neighbouring town to high PM2.5 concentrations during the sugarcane harvest period. This exposure was higher among the sugarcane workers, as illustrated by both higher PM2.5 concentrations in the sugarcane fields and higher urinary 1-hydroxypyrene levels in the volunteers in this group. The higher incidence of respiratory symptoms, greater decrease in lung function and more marked elevation of oxidative stress markers among the sugarcane workers during the harvest confirms the greater effect magnitude in this population and a dose-dependent relationship between pollution and the observed effects. (C) 2012 Elsevier B.V. All rights reserved.