S Nitrosothiol
Mostrando 1-12 de 31 artigos, teses e dissertações.
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1. Effects of oral administration of S-nitrosothiols and knectic evaluation of the kinetic propensity and resistance to diet induced obessity / Efeitos da administração orogástrica de s-nitrosotióis e avaliação cinética da propensão e resistência à obsidade induzida por dieta
In the present study, the nitric oxide (NO)-associated physiological actions obtained topically on the gastric mucosa and systemically in oral administrations of two NO donors-S-nitrosothiols (RSNOs), S-nitrosoglutathione (GSNO) and S-nitroso-N-acetylcysteine (SNAC) were investigated in animal models. The topical ex vivo administration of RSNOs solutions on
IBICT - Instituto Brasileiro de Informação em Ciência e Tecnologia. Publicado em: 15/07/2011
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2. Glutathione and the redox control system trypanothione/trypanothione reductase are involved in the protection of Leishmania spp. against nitrosothiol-induced cytotoxicity
Glutathione is the major intracellular antioxidant thiol protecting mammalian cells against oxidative stress induced by oxygen- and nitrogen-derived reactive species. In trypanosomes and leishmanias, trypanothione plays a central role in parasite protection against mammalian host defence systems by recycling trypanothione disulphide by the enzyme trypanothio
Brazilian Journal of Medical and Biological Research. Publicado em: 2006-03
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3. Anti-inflamatory effect of the S-nitroso-N-acetyleysteine (SNAC) on left ventricular hypertrophy in hypercholesterolemic LDLr/mice / Efeito antiinflamatorio da S-nitroso-N-acetilcisteina (SNAC) na hipertrofia ventricular esquerda (HVE) em camundongos hipercolesterolemicos knockout para o receptor de LDL (LDLr-/-)
Recently, it has been that S-nitroso-N-acetylcysteine (SNAC) attenuate in 55% the plaque development in low-density lipoprotein-receptor-deficient (LDLr-/-) mice fed a hypercholesterolemic diet for 15 days. The present study was designed to verify whether deletion of the low-density lipoprotein (LDL) receptor gene may affect the hemodynamic profile and adren
Publicado em: 2006
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4. Efeito antiinflamatorio da S-nitroso-N-acetilcisteina (SNAC) na aterogenese em camundongos
Background: Several inflammatory pathways have been shown to participate in the atherosclerotic process. Different markers for inflammation and endothelial dysfunction have been found to predict the future risk for developing cardiovascular disease. Newer markers such as CD40 ligand appear to provide important information regarding clinical risk. In hypercho
Publicado em: 2005
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5. Nitric oxide release from the S-nitrosothiol zinc phthalocyanine complex by flash photolysis
The photogeneration of nitric oxide (NO) using laser flash photolysis was investigated for S-nitroso-glutathione (GSNO) and S-nitroso-N-acetylcysteine (NacySNO) at pH 6.4 (PBS/HCl) and 7.4 (PBS). Irradiation of S-nitrosothiol with light (lambda = 355 nm followed by absorption spectroscopy) resulted in the homolytic decomposition of NacySNO and GSNO to genera
Brazilian Journal of Medical and Biological Research. Publicado em: 2003-05
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6. Lipid peroxidation and nitric oxide inactivation in postmenopausal women
OBJECTIVE: To assess the effect of endogenous estrogens on the bioavailability of nitric oxide (·NO) and in the formation of lipid peroxidation products in pre- and postmenopausal women. METHODS: NOx and S-nitrosothiols were determined by gaseous phase chemiluminescence, nitrotyrosine was determined by ELISA, COx (cholesterol oxides) by gas chromatography,
Arquivos Brasileiros de Cardiologia. Publicado em: 2003-04
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7. Prevenção das disfunções vasculares no inicio da aterogenese : efeito da S-Nitroso-N-Acetilcisteina, SNAC, em camundongos knock out para o receptor da LDL
Pathophysiology of the NO/NO synthase system and endothelium dysfunctional changes in early phases of the atherogenic process are incompletely understood. In hypercholesterolemic LDLr-/- mice, we addressed changes in endothelium-dependent relaxations, NO synthase expression and plaque burden in the absence or presence of the nitrosothiol NO donor S-nitroso-N
Publicado em: 2003
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8. The mechanism of transmembrane S-nitrosothiol transport
S-nitrosothiols have been suggested to play an important role in nitric oxide (NO)-mediated biological events. However, the mechanisms by which an S-nitrosothiol (or the S-nitroso functional group) is transferred across cell membrane are still poorly understood. We have demonstrated previously that the degradation of S-nitrosoglutathione (GSNO) by cells abso
National Academy of Sciences.
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9. Inhibition of Bacillus cereus spore outgrowth by covalent modification of a sulfhydryl group by nitrosothiol and iodoacetate.
Nitrosothiols with the general structure RSN==O were studied as a model system of bacteriostatic action toward outgrowing bacterial spores. With a Taft plot analysis, the influence of the structure of the R group on the inhibitory effectiveness of a series of nitrosothiols showed that effectiveness as an inhibitor of Bacillus cereus T outgrowth correlated wi
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10. Nitric oxide reacts with intracellular glutathione and activates the hexose monophosphate shunt in human neutrophils: evidence for S-nitrosoglutathione as a bioactive intermediary.
We performed experiments to determine whether nitric oxide promoted the formation of intracellular S-nitrosothiol adducts in human neutrophils. At concentrations sufficient to inhibit chemoattractant-induced superoxide anion production, nitric oxide caused a depletion of measurable intracellular glutathione as determined by both the monobromobimane HPLC meth
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11. Inhibition of neointimal proliferation in rabbits after vascular injury by a single treatment with a protein adduct of nitric oxide.
Endothelium-derived relaxing factor is important for vascular homeostasis and possesses qualities that may modulate vascular injury, including vasodilation, platelet inhibition, and inhibition of smooth muscle proliferation. S-nitrososerum albumin is a naturally occurring adduct of nitric oxide (NO) with a prolonged biologic half-life and is a potent vasodil
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12. Cell-surface protein disulfide isomerase catalyzes transnitrosation and regulates intracellular transfer of nitric oxide
Since thiols can undergo nitrosation and the cell membrane is rich in thiol-containing proteins, we considered the possibility that membrane surface thiols may regulate cellular entry of NO. Recently, protein disulfide isomerase (PDI), a protein that catalyzes thio–disulfide exchange reactions, has been found on the cell-surface membrane. We hypothesized t
American Society for Clinical Investigation.