Navegando por Palavras-chave "hydrogen peroxide"
Agora exibindo 1 - 5 de 5
Resultados por página
Opções de Ordenação
- ItemSomente MetadadadosCardiovascular responses produced by central injection of hydrogen peroxide in conscious rats(Elsevier B.V., 2006-12-11) Cardoso, Leonardo Maximo; Colombari, Debora Simoes de Almeida; Menani, Jose Vanderlei; Chianca, Deoclecio Alves; Colombari, Eduardo; Universidade Federal de São Paulo (UNIFESP); UFOPReactive oxygen species (ROS) have been shown to modulate neuronal synaptic transmission and may play a role on the autonomic control of the cardiovascular system. in this study we investigated the effects produced by hydrogen peroxide (H2O2) injected alone or combined with the anti-oxidant agent N-acetil-L-Cysteine (NAC) or catalase into the fourth brain ventricle (4th V) on mean arterial pressure and heart rate of conscious rats. Moreover the involvement of the autonomic nervous system on the cardiovascular responses to H2O2 into the 4th V was also investigated. Male Holtzman rats (280-320g) with a stainless steel cannula implanted into the 4th V and polyethylene carmulas inserted into the femoral artery and vein were used. Injections of H202 (0.5, 1.0 and 1.5 mu mol/0.2 mu L, n = 6) into the 4th V produced transient (for 10 min) dose-dependent pressor responses. the 1.0 and 1.5 mu mol doses of H2O2 also produced a long lasting bradycardia (at least 24 h with the high dose of H2O2). Prior injection of N-acetyl-L-cysteine (250 nmol/1 mu L/rat) into the 4th V blockade the pressor response and attenuated the bradycardic response to H2O2 (1 mu mol/0.5 mu L/rat, n = 7) into the 4th V. Intravenous (i.v.) atropine methyl bromide (1.0 mg/kg, n = 11) abolished the bradycardia but did not affect the pressor response to H2O2. Prazosin hydrochloride (1.0 mg/kg, n = 6) i.v. abolished the pressor response but did not affect the bradycardia. the increase in the catalase activity (500 UEA/1 mu L/rat injected into the 4th V) also abolished both, pressor and bradycardic responses to H2O2. the results suggest that increased ROS availability into 4th V simultaneously activate sympathetic and parasympathetic outflow inducing pressor and bradycardic responses. (c) 2006 Elsevier Inc. All rights reserved.
- ItemSomente MetadadadosCytotoxicity of 1,4-diamino-2-butanone, a putrescine analogue, to RKO cells: mechanism and redox imbalance(Informa Healthcare, 2013-09-01) Soares, C. O.; Boiani, M.; Marnett, L. J.; Bechara, E. J. H. [UNIFESP]; Universidade de São Paulo (USP); Vanderbilt Univ; Universidade Federal de São Paulo (UNIFESP)alpha-Aminocarbonyl metabolites (e.g., 5-aminolevulinic acid and aminoacetone) and the wide spectrum microbicide 1,4-diamino-2-butanone (DAB) have been shown to exhibit pro-oxidant properties. in vitro, these compounds undergo phosphate-catalyzed enolization at physiological pH and subsequent superoxide radical-propagated aerobic oxidation, yielding a reactive alpha-oxoaldehyde and H2O2. DAB cytotoxicity to pathogenic microorganisms has been attributed to the inhibition of polyamine biosynthesis. However, the role played in cell death by reactive DAB oxidation products is still poorly understood. This work aims to clarify the mechanism of DAB-promoted pro-oxidant action on mammalian cells. DAB (0.05-10 mM) treatment of RKO cells derived from human colon carcinoma led to a decrease in cell viability (IC50 ca. 0.3 mM DAB, 24 h incubation). Pre-addition of either catalase (5 mu M) or aminoguanidine (20 mM) was observed to partially inhibit the toxic effects of DAB to the cells, while N-acetyl-L-cysteine (NAC, 5 mM) or reduced glutathione (GSH, 5 mM) provided almost complete protection against DAB. Changes in redox balance and stress response pathways were indicated by the increased expression of HO-1, NQO1 and xCT. Moreover, the observation of caspase 3 and PARP cleavage products is consistent with DAB-triggered apoptosis in RKO cells, which was corroborated by the partial protection afforded by the pan-caspase inhibitor z-VAD-FMK. Finally, DAB treatment disrupted the cell cycle in response to increased p53 and activation of ATM. Altogether, these data support the hypothesis that DAB exerts cytotoxicity via a mechanism involving not only polyamine biosynthesis but also by DAB oxidation products.
- ItemSomente MetadadadosEffect of montelukast on exhaled nitric oxide and nonvolatile markers of inflammation in mild asthma(Amer Coll Chest Physicians, 2003-10-01) Sandrini, A.; Ferreira, I. M.; Gutierrez, C.; Jardim, Jose R. [UNIFESP]; Zamel, N.; Chapman, K. R.; Univ Toronto; Toronto Western Hosp; Universidade Federal de São Paulo (UNIFESP)Study objectives: Leukotriene receptor antagonists appear to exert anti-inflammatory activity in asthma. We undertook the present study to evaluate the effect of montelukast on levels of exhaled nitric oxide (ENO) and two inflammatory markers, hydrogen peroxide (H2O2), and cysteinyl. leukotrienes (cys-LTs), in the exhaled breath condensate of subjects with mild asthma.Patients: Twenty stable subjects with mild asthma (15 women and 5 men; mean [+/-SD] age, 34.8 +/- 12.6 years) were included in the study. Intervention: A 1-week run-in period was followed by 2 weeks of treatment (with montelukast or placebo) that was administered in randomized, double-blind, crossover fashion. One week of washout followed each treatment arm.Results: Montelukast significantly reduced the levels of ENO from baseline (median, 52.5 parts per billion [ppb]; 25th to 75th percentile, 37.8 to 101.8 ppb) during the entire treatment period (ie, day 1 to day 14), with the effect measurable as early as day I (median, 45.9 ppb; 25th to 75th percentile, 29.3 to 92.5 ppb) and with the maximal effect being observed on day 7 (median, 35.7 ppb; 25th to 75th percentile, 27.6 to 66.6 ppb). the levels of ENO did not change significantly with placebo therapy. Montelukast improved symptom score and reduced peak expiratory flow (PEF) variability. Changes in PEF variability correlated positively with changes in ENO (r = 0.46; p = 0.04). No significant changes in FEV1 or concentration of H2O2 in the exhaled breath condensate were observed. Levels of cys-LTs were undetectable in the exhaled breath condensate.Conclusions: We concluded that montelukast reduces the levels of ENO in patients with mild asthma, a finding that is compatible with an anti-inflammatory effect of montelukast, and that ENO appears to be more sensitive in detecting this effect, than FEV1 and H2O2 levels in the exhaled breath condensate.
- ItemSomente MetadadadosExpression of the selectable marker gene bsrm in BALB/MK cells induces apoptosis by overproduction of hydrogen peroxide(Natl Research Council Canada-n R C Research Press, 2007-10-01) Takeshita, Daniela; Bento, Fernanda Mara; Chammas, Roger; Belizario, Jose Ernesto; Carmona, Adriana Karaoglanovic; Konno, Katsuhiro; Melo, Robson Lopes de; Molina, Gustavo; Lisboa, Bianca Cristina Garcia; Han, Sang Won [UNIFESP]; Universidade Federal de São Paulo (UNIFESP); Universidade de São Paulo (USP); Butantan InstTransduction of the retroviral vector LBmSN, which expresses the blasticidin S resistance gene bsrm in the murine keratinocyte cell line BALB/MK, induces death in these cells. Cell death is caused by a factor called DOKEB (death factor obtained from keratinocytes expressing bsrm), which is released before the cells' death. in this report we describe and discuss the purification and characterization of DOKEB. Our results were as follows. (i) the 5-day-old medium from the modified BALB/MK cells with LBmSN was used for purification and characterization by filtration and chromatography: DOKEB was a stable and highly hydrophilic compound, with a molecular mass less than that of I amino acid. (ii) the conditioned medium containing DOKEB was reactive against thiobarbituric acid and dichlorofluorescein diacetate. (iii) DOKEB activity was neutralized by the incubation of the conditioned medium with catalase. Therefore, our conclusion is that the BALB/MK cells expressing bsrm produce a large amount of hydrogen peroxide, which catalyzes the process of apoptosis of those cells.
- ItemAcesso aberto (Open Access)Redox modulation of thimet oligopeptidase activity by hydrogen peroxide(Wiley, 2017) Icimoto, Marcelo Y. [UNIFESP]; Ferreira, Juliana C.; Yokomizo, Cesar H.; Bim, Larissa V. [UNIFESP]; Marem, Alyne [UNIFESP]; Gilio, Joyce M. [UNIFESP]; Oliveira, Vitor [UIFESP]; Nantes, Iseli L.Thimet oligopeptidase (EC 3.4.24.15, TOP) is a cytosolic mammalian zinc protease that can process a diversity of bioactive peptides. TOP has been pointed out as one of the main postproteasomal enzymes that process peptide antigens in the MHC class I presentation route. In the present study, we describe a fine regulation of TOP activity by hydrogen peroxide (H2O2). Cells from a human embryonic kidney cell line (HEK293) underwent an ischemia/reoxygenation-like condition known to increase H2O2 production. Immediately after reoxygenation, HEK293 cells exhibited a 32% increase in TOP activity, but no TOP activity was observed 2 h after reoxygenation. In another model, recombinant rat TOP (rTOP) was challenged by H2O2 produced by rat liver mitoplasts (RLMt) alone, and in combination with antimycin A, succinate, and antimycin A plus succinate. In these conditions, rTOP activity increased 17, 30, 32 and 38%, respectively. Determination of H2O2 concentration generated in reoxygenated cells and mitoplasts suggested a possible modulation of rTOP activity dependent on the concentration of H2O2. The measure of pure rTOP activity as a function of H2O2 concentration corroborated this hypothesis. The data fitted to an asymmetrical bell-shaped curve in which the optimal activating H2O2 concentration was 1.2 nM, and the maximal inhibition (75% about the control) was 1 mu M. Contrary to the oxidation produced by aging associated with enzyme oligomerization and inhibition, H2O2 oxidation produced sulfenic acid and maintained rTOP in the monomeric form. Consistent with the involvement of rTOP in a signaling redox cascade, the H2O2-oxidized rTOP reacted with dimeric thioredoxin-1 (TRx-1) and remained covalently bound to one subunit of TRx-1.