80 resultados para INDUCED LOCAL OXIDATION
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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
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Background: the incidence of gingival overgrowth (GO) associated with the use of cyclosporin A (CsA) is controversial. In the present study, we determined the incidence of GO in Brazilian renal transplant patients treated with CsA and the possible associations between periodontal and pharmacological variables.Methods: the test group consisted of 20 renal transplant patients, and the control group included 20 non-transplant patients. Periodontal conditions were evaluated based on the plaque index (PI), gingival index (GI), probing depth (PD), and the rate of gingival overgrowth, together with pharmacological variables (daily CsA dose and duration of treatment).Results: A significant difference in PI (P<0.0001) and PD (P<0.0001) was observed between groups, while GI (P=0.15) did not differ significantly. Using the Pearson correlation coefficient, a significant correlation was observed not only between GI (P<0.001; r=0.8141) and GO, but also for PD (P<0.001; r=0.866) and GO. The other correlations were not statistically significant.Conclusions: We conclude that GO induced by CsA may vary according to the individual sensitivity of each patient and may or may not be correlated with other local factors (periodontal variables).
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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
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Myonecrosis with permanent loss of muscle mass is a relevant local toxic effect following envenomation with Bothrops jararacussu snake venom. Regeneration of adult skeletal muscle involves the activation of satellite cells, a process regulated by myogenic regulatory factors (MRF). MyoD is an MRF involved in both proliferation and differentiation of satellite cells. Androgens are modulators of skeletal muscle, known to increase muscle mass and strength. This study examined the hypothesis that anabolic androgens improve the muscle regeneration process in mice following envenomation by Bothrops jararacussu snake venom. Myonecrosis was induced by venom injection (30 g/50 l in physiological solution) over the extensor digitorum longus (EDL) muscles of mice. Nandrolone (ND) (6 mg/kg, sc) was administered after 12 h, 7 d, and 14 d following venom injection. The histological changes in EDL muscle at 1, 3, 7, and 21 d after muscle injury were analyzed by light microscopy. Cross-sectional areas of fibers were measured. MyoD was evaluated by immunofluorescence technique. Histological examination revealed the presence of a regeneration process in ND-treated animals, characterized by the appearance of some myotubes at 3 d, and numerous myotubes at 7 d from venom injection. Nandrolone treatment reduced the frequency of small fibers at 7 and 21 d after venom administration, and increased the frequency of large fibers at 7 d postinjury. Nandrolone also significantly augmented the expression of MyoD-positive cells at 7 and 21 d after envenomation. These results suggest that ND accelerates muscle regeneration and indicate the involvement of MyoD in this process.
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Alcoholism is rampant in modern society and some antioxidant compound could perhaps be useful to reduce the damage done by alcohol consumption and abstinence. The present study was undertaken to investigate the association of N-acetylcysteine (NAC) intake, alcoholism, and alcohol abstinence on lipid profile, in vivo low-density lipoprotein (LDL) oxidation, oxidative stress, and antioxidant status in serum and liver of rats. Initially, male Wistar 30 rats were divided into two groups: (C, N = 6) given standard chow and water; (E, N = 24) receiving standard chow and aqueous ethanol solution in semi-voluntary research. After 30 days of ethanol exposure, (E) group was divided into four subgroups (N = 6/group): (E-E) continued drinking 30% ethanol solution; (E-NAC) drinking ethanol solution containing 2 g/L NAC (AB) changed ethanol solution to water; (AB-NAC) changed ethanol to aqueous solution 2 g/L NAC. After 15 days of the E-group division, E-E rats had higher serum alanine transaminase, lower body weight, and surface area, despite higher energy intake than C. E-E rats had also lower feed efficiency, dyslipidemia with enhanced triacyl glycerol, very low-density lipoprotein (VLDL), lipid hydroperoxide (LH) and in vivo oxidized-LDL (ox-LDL). AB, E-NAC, and AB-NAC rats ameliorated serum oxidative stress markers and normalized serum lipids. E-E rats had higher hepatic LH and lower reduced glutathione (GSH)/oxidized glutathione (GSSG) ratio than C, indicating hepatic oxidative stress. AB and E-NAC rats normalized hepatic LH, GSSG, and the GSH/GSSG ratio, compared to E-E. AB-NAC rats had the lowest serum ox-LDL, hepatic LH levels, and the highest GSH reductase activity in hepatic tissue. In conclusion, the present study brought new insights into alcohol consumption, because ethanol exposure enhanced serum in vivo ox-LDL, as well as serum and hepatic oxidative stress. N-acetylcysteine offers promising therapeutic value to inhibit ethanol-induced adverse effects. Ethanol withdrawal had beneficial effects on serum lipids, but was more effective when coupled with NAC supplementation. Ethanol abstinence and NAC intake interact synergistically, improving serum lipids and hepatic antioxidant defenses. (c) 2009 Elsevier B.V. All rights reserved.
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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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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
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Injetou-se lidocaína (100mg 2%) na articulação do carpo para avaliar a resposta inflamatória induzida pela injeção (1,5ng) intra-articular de lipopolissacarídeo (LPS) de E. coli. Utilizaram-se 17 cavalos Mangalarga não castrados, entre dois e três anos, divididos em três grupos. No carpo esquerdo (CE) administrou-se solução fisiológica a 0,9% (SAL) e no carpo direito (CD) uma das seguintes combinações: grupo A (n=6) LPS mais SAL, grupo B (n=6) LPS mais lidocaína e grupo C (n=5) lidocaína mais SAL. Amostras do líquido sinovial e de sangue foram colhidas imediatamente antes da injeção de LPS (T0) e às 1,30 (T1), 3 (T2), 6 (T3), 12 (T4) e 36 horas (T5) após a injeção. Variáveis clínicas e físicas, e características bioquímicas e celulares do líquido sinovial foram avaliadas nos mesmos tempos. A resposta inflamatória local e sistêmica foi mensurada pela concentração do TNF-alfa no soro e líquido sinovial. Observou-se aumento da concentração do TNF-alfa nas articulações injetadas com LPS às 3h no grupo A e de 1,30 às 3h no grupo B. Concluiu-se que o LPS induziu o processo inflamatório e que a lidocaína não inibiu nem atenuou a sinovite induzida pelo LPS, nem a síntese e liberação de TNF-alfa .
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Pradosia huberi is a medicinal plant very common in the Amazonian forest population. The research interest in this plant is justifiable because of its potential medicinal value in gastritis and gastric ulcer mentioned in local folk medicine. In this paper, we evaluated the acute toxicity and antiulcerogenic effect of a hydroalcoholic extract (HAE) obtained from Pradosia huberi barks in rodents. No acute toxicological sign or symptom was observed in animals treated with the highest dose (5000 mg/kg, p.o.) of Pradosia huberi. In the HCl/EtOH-induced gastric ulcer model, HAE demonstrated significant inhibition of the ulcerative lesion index by 73% (500 mg/kg) and 88% (1000 mg/kg), respectively, in relation to the control value (p < 0.05). The gastric damage induced by absolute ethanol in rats was effectively reduced by 84, 88 and 81% (250, 500 and 1000 mg/kg) when compared with the control group (p < 0.01). In the NSAID-induced lesion model, HAE also showed antiulcerogenic effect with decrease in gastric lesions of 56% (250 mg/kg), 57% (500 mg/kg) and 67% (1000 mg/kg) when compared with animals treated with vehicle (p < 0.05). In the gastric ulcer induced by pylorus ligature model, the administration of HAE by oral and intraduodenal routes inhibited the gastric lesion index by 79 and 52% (500 mg/kg), respectively. HAE administered orally or intraduodenally was able to change gastric juice parameters (pH, volume and acid output) as well as those treated with cimetidine. The treatment with HAE (p.o.) significantly increased gastric volume, the pH values and promoted reduced acid output (1) < 0.01). By comparative effect (intraduodenal and oral route), we observed that HAE was better for local activity in gastric mucosa than in systemic action. HAE also has a non-specific activity when found to be the inhibitor of intestinal motility (p > 0.01). The mechanism of action of HAE did not seem to be related to the NO-inhibitor but showed the participation of endogenous sulphydryl group in the gastroprotective action. (C) 2005 Elsevier B.V.. All rights reserved.
Kinetics and mechanism of the induced redox reaction of [Ni(cyclam)](2+) promoted by SO5 center dot-
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Oxidation of [Ni(cyclam)](2+), cyclam = 1,4,8,11-tetraazacyclotetradecane, accelerated by sulfur dioxide, was studied spectrophotometrically by following the formation of [Ni(cyclam)](3+) under the conditions: [Ni(cyclam)](2+) = 6.0 x 10(-3) M; initial [Ni(cyclam)](3+) = 8.0 x 10(-6) M; [cyclam] = 6.0 x 10(-3) M; [SO2] = (1.0-5.0) x 10(-4) M and 1.0 M perchloric acid in oxygen saturated solutions at 25.0 degrees C and ionic strength = 1.0 M. The oxidation reaction exhibits autocatalytic behavior in which the induction period depends on the initial Ni(III) concentration. A kinetic study of the reduction of Ni(III) by SO2 under anaerobic conditions, and the oxidation of Ni(II), showed that the rate-determining step involves reduction of Ni(III) by SO2 to produce the SO3.- radical, which rapidly reacts with dissolved oxygen to produce SO5.- and rapidly oxidizes Ni(II). The results clearly show a redox cycling process which depends on the balance of SO2 and oxygen concentrations in solution.