Dmtu
Mostrando 1-11 de 11 artigos, teses e dissertações.
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1. Avaliação do estresse oxidativo e estado redox mitocondrial na hepatotoxicidade induzida pela cisplatina em ratos Wistar: efeito protetor da dimetiltiouréia / Evaluation of mitochondrial oxidative stress and redox state in the cisplatin-induced hepatotoxicity in Wistar rats: protective effect of dimethylthiourea
Cisplatin is still one of the most effective chemotherapeutic agents. However, at higher doses hepatotoxicity may occur. Some antioxidants have been shown to ameliorate cisplatin-induced hepatotoxicity but the involved molecular mechanism has not been clarified. In the present study we investigated the molecular mechanism underlying the protective effect of
Publicado em: 2007
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2. ?Effect of cisplatin on the function, oxidative stress and renal mitochondrial redox state / Efeito da cisplatina na função, estresse oxidativo e estado redox mitocondrial renal em ratos: efeito protetor da dimetiltiouréia
Embora a cisplatina (cis-diaminocloroplatina II) seja um efetivo agente anticâncer, seu uso clínico é altamente limitado, predominantemente devido ao seu potencial nefrotóxico. Muitos estudos têm demonstrado que a cisplatina causa disfunção mitocondrial em células epiteliais renais e danos ao DNA nuclear devido à ação de espécies reativas de oxig
Publicado em: 2006
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3. Prevention of granulocyte-mediated oxidant lung injury in rats by a hydroxyl radical scavenger, dimethylthiourea.
Toxic, partially reduced metabolites of oxygen (toxic oxygen radicals) are increasingly implicated in acute leukocyte-mediated tissue injury. To further probe the roles of oxygen radicals in acute lung edema, I studied the effects of a recently described and very potent oxygen radical scavenger, dimethylthiourea (DMTU) (Fox, R. B., R. N. Harada, R. M. Tate,
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4. Evidence suggesting a role for hydroxyl radical in gentamicin-induced acute renal failure in rats.
The protective effect of hydroxyl radical scavengers and iron chelators has strongly implicated the hydroxyl radical in several models of tissue injury. Based on in vitro studies showing gentamicin-enhanced generation of reactive oxygen metabolites in renal cortical mitochondria, we examined the effect of hydroxyl radical scavengers and iron chelators in gen
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5. Effects of inorganic iron and myoglobin on in vitro proximal tubular lipid peroxidation and cytotoxicity.
Recent in vivo studies suggest that heme Fe causes proximal tubular lipid peroxidation and cytotoxicity, thereby contributing to the pathogenesis of myoglobinuric (Mgb) acute renal failure. Because hydroxyl radical (.OH) scavengers [dimethylthiourea (DMTU), benzoate, mannitol] can mitigate this injury, it is postulated that .OH is a mediator of Mgb-induced r
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6. Xanthine oxidase produces hydrogen peroxide which contributes to reperfusion injury of ischemic, isolated, perfused rat hearts.
Three lines of investigation indicated that hydrogen peroxide (H2O2) from xanthine oxidase (XO) contributes to cardiac dysfunction during reperfusion after ischemia. First, addition of dimethylthiourea (DMTU), a highly permeant O2 metabolite scavenger (but not urea) simultaneously with reperfusion improved recovery of ventricular function as assessed by vent
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7. Oxygen free radicals in ischemic acute renal failure in the rat.
During renal ischemia, ATP is degraded to hypoxanthine. When xanthine oxidase converts hypoxanthine to xanthine in the presence of molecular oxygen, superoxide radical (O-2) is generated. We studied the role of O-2 and its reduction product OH X in mediating renal injury after ischemia. Male Sprague-Dawley rats underwent right nephrectomy followed by 60 min
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8. Xanthine oxidase-derived hydrogen peroxide contributes to ischemia reperfusion-induced edema in gerbil brains.
The contribution of toxic O2 metabolites to cerebral ischemia reperfusion injury has not been determined. We found that gerbils subjected to temporary unilateral carotid artery occlusion (ischemia) consistently developed neurologic deficits during ischemia with severities that correlated with increasing degrees of brain edema and brain H2O2 levels after repe
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9. The as-1 Promoter Element Is an Oxidative Stress-Responsive Element and Salicylic Acid Activates It via Oxidative Species1
The activation sequence-1 (as-1)-like element found in the promoter of some glutathione S-transferase (GST) genes, has been previously described as a salicylic acid (SA)- and auxin-responsive element. In this paper, we tested the hypothesis that the activating effect of SA on the as-1 element is mediated by oxidative species. Supporting this hypothesis, our
American Society of Plant Biologists.
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10. Oxygen radicals as second messengers for expression of the monocyte chemoattractant protein, JE/MCP-1, and the monocyte colony-stimulating factor, CSF-1, in response to tumor necrosis factor-alpha and immunoglobulin G. Evidence for involvement of reduced nicotinamide adenine dinucleotide phosphate (NADPH)-dependent oxidase.
The potential involvement of reactive oxygen species in the expression of genes involved in immune response was examined in mesangial cells. Tumor necrosis factor (TNF-alpha) and aggregated (aggr.) IgG increased mRNA levels for the monocyte chemoattractant protein, JE/MCP-1, and the colony-stimulating factor, CSF-1. Scavengers for free radicals such as di- a
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11. Mechanism of oxidative stress-induced intracellular acidosis in rat cerebellar astrocytes and C6 glioma cells.
1. Following ischaemic reperfusion, large amounts of superoxide anion (.O2-), hydroxyl radical (.OH) and H2O2 are produced, resulting in brain oedema and changes in cerebral vascular permeability. We have found that H2O2 (100 microM) induces a significant intracellular acidosis in both cultured rat cerebellar astrocytes (0.37 +/- 0.04 pH units) and C6 glioma