Showing papers on "Hydrogen peroxide published in 1997"
TL;DR: In vitro and in vivo results provide genetic evidence that up-regulation of Hmox1 serves as an adaptive mechanism to protect cells from oxidative damage during stress.
Abstract: Stressed mammalian cells up-regulate heme oxygenase 1 (Hmox1; EC 1.14.99.3), which catabolizes heme to biliverdin, carbon monoxide, and free iron. To assess the potential role of Hmox1 in cellular antioxidant defense, we analyzed the responses of cells from mice lacking functional Hmox1 to oxidative challenges. Cultured Hmox1−/− embryonic fibroblasts demonstrated high oxygen free radical production when exposed to hemin, hydrogen peroxide, paraquat, or cadmium chloride, and they were hypersensitive to cytotoxicity caused by hemin and hydrogen peroxide. Furthermore, young adult Hmox1−/− mice were vulnerable to mortality and hepatic necrosis when challenged with endotoxin. Our in vitro and in vivo results provide genetic evidence that up-regulation of Hmox1 serves as an adaptive mechanism to protect cells from oxidative damage during stress.
1,268 citations
TL;DR: It is suggested that mitochondria are a target of ceramide produced in the signaling of TNF whose effect on mitochondrial electron transport chain leads to overproduction of hydrogen peroxide and consequently this phenomena may account for the generation of reactive oxygen species during TNF cytotoxicity.
791 citations
TL;DR: The physiological implications of cells having to maintain a reducing environment during apoptosis to allow the caspases to function are discussed and hydrogen peroxide has two distinct effects.
666 citations
TL;DR: This study introduces a simple direct antioxidant assay, based on the reduction of the ABTS, and compares it with the myoglobin/ABTS, establishing that the antioxidants studied to date in the latter assay act by scavenging the AB TS.
Abstract: (1997). Factors Influencing the Antioxidant Activity Determined by the ABTS•+ Radical Cation Assay. Free Radical Research: Vol. 26, No. 3, pp. 195-199.
655 citations
TL;DR: The role of active oxygen species in the photocatalytic bactericidal effect was investigated using a thin transparent titanium dioxide (TiO2) film, and the viable number of Escherichia coli (E. coli) significantly decreased on the illuminated TiO2 film as mentioned in this paper.
Abstract: The role of active oxygen species in the photocatalytic bactericidal effect was investigated using a thin transparent titanium dioxide (TiO2) film. The viable number of Escherichia coli (E. coli) significantly decreased on the illuminated TiO2 film, and the bactericidal effect was observed even when E. coli was separated from the TiO2 surface with a 50 μm porous membrane. Mannitol, a hydroxyl radical scavenger, inhibited the effect only in the absence of the membrane. In contrast, catalase inhibited the effect in all cases. On the basis of these results, the long-range bactericidal effect of hydrogen peroxide was proposed, together with a cooperative effect due to other oxygen species. © 1997 Elsevier Science S.A.
626 citations
TL;DR: The cytotoxic effects of O2 .
575 citations
TL;DR: Quantitative analysis indicated a prolonged burst of H2O2 occurring between 5 to 8 hr after inoculation in cells undergoing the HR during this example of non-host resistance, which is consistent with its direct role as an antimicrobial agent and as the cause of localized membrane damage at sites of bacterial attachment.
Abstract: The active oxygen species hydrogen peroxide (H2O2) was detected cytochemically by its reaction with cerium chloride to produce electron-dense deposits of cerium perhydroxides. In uninoculated lettuce leaves, H2O2 was typically present within the secondary thickened walls of xylem vessels. Inoculation with wild-type cells of Pseudomonas syringae pv phaseolicola caused a rapid hypersensitive reaction (HR) during which highly localized accumulation of H2O2 was found in plant cell walls adjacent to attached bacteria. Quantitative analysis indicated a prolonged burst of H2O2 occurring between 5 to 8 hr after inoculation in cells undergoing the HR during this example of non-host resistance. Cell wall alterations and papilla deposition, which occurred in response to both the wild-type strain and a nonpathogenic hrpD mutant, were not associated with intense staining for H2O2, unless the responding cell was undergoing the HR. Catalase treatment to decompose H2O2 almost entirely eliminated staining, but 3-amino-1,2,4-triazole (catalase inhibitor) did not affect the pattern of distribution of H2O2 detected. H2O2 production was reduced more by the inhibition of plant peroxidases (with potassium cyanide and sodium azide) than by inhibition of neutrophil-like NADPH oxidase (with diphenylene iodonium chloride). Results suggest that CeCl3 reacts with excess H2O2 that is not rapidly metabolized during cross-linking reactions occurring in cell walls; such an excess of H2O2 in the early stages of the plant-bacterium interaction was only produced during the HR. The highly localized accumulation of H2O2 is consistent with its direct role as an antimicrobial agent and as the cause of localized membrane damage at sites of bacterial attachment.
518 citations
Journal Article•
TL;DR: The overall results support the possibility that a particles, at least in part, may mediate their DNA-damaging effects indirectly via a ROS-related mechanism.
Abstract: The mechanism(s) by which high-linear energy transfer α particles, like those emitted by inhaled radon and radon daughters, cause lung cancer has not been elucidated. Conceivably, DNA damage that is induced by α particles may be mediated by the metabolic generation of reactive oxygen species (ROS), in addition to direct α particle-DNA interactions and hydroxyl radical-DNA interactions. Using normal human lung fibroblasts, we investigated the hypothesis that densely ionizing α particles may induce the intracellular generation of superoxide (O2·-) and hydrogen peroxide (H2O2). Ethidium bromide and 2′,7′-dichlorofluorescein, fluorescent products of the membrane-permeable dyes hydroethidine and 2′,7′-dichlorofluorescin diacetate, respectively, were used to monitor the intracellular production of O2·- and H2O2, respectively, by flow cytometry. Compared to sham-irradiated cells, fibroblasts that were exposed to α particles (0.4–19 cGy) had significant increases in intracellular O2·- production, along with concomitant increases in H2O2 production. Further analyses suggest that the plasma membrane-bound NADPH-oxidase is primarily responsible for this increased intracellular generation of ROS and that the ROS response does not require direct nuclear or cellular “hits” by the α particles. In this latter regard, we additionally report that unirradiated cells also show the ROS response when they are incubated with serum-containing culture medium that has been exposed to α particles or when they are incubated with supernatants from α-irradiated cells. Our overall results support the possibility that α particles, at least in part, may mediate their DNA-damaging effects indirectly via a ROS-related mechanism.
444 citations
TL;DR: A review of information related to low molecular weight metal chelators isolated from wood decay fungi is presented in this paper, where the presence of the chelator in wood degraded by G. trabeum has been demonstrated by ELISA and TEM immunolabelling studies.
419 citations
TL;DR: In this paper, the mechanism of photo-oxidation of natural dissolved organic matter (DOM) in the presence of iron was examined in laboratory model systems containing fulvic acid and lepidocrocite (γ-FeOOH) particles.
Abstract: The purpose of this study is to examine the mechanism of photo-oxidation of natural dissolved organic matter (DOM) in the presence of iron. This process is of interest in natural waters for several reasons: as a significant sink of DOM in sunlit surface waters; as a source and sink of reactive oxygen species (HO2/O2•-, hydrogen peroxide, and HO•) and as a factor controlling iron speciation. Studies were conducted in laboratory model systems containing fulvic acid and lepidocrocite (γ-FeOOH) particles at pH 3 and pH 5, irradiated with simulated sunlight. Measured concentrations of dissolved Fe(II), total dissolved Fe, and hydrogen peroxide were interpreted as the net effects of competing reactions reducing and oxidizing Fe and producing and destroying hydrogen peroxide. A kinetic model constructed using information gained from separate experiments in simpler systems was used to assess the relative importance of individual reactions. Comparison of photoreductive dissolution rates in aerated and de-aerated ...
398 citations
TL;DR: The trapped hydroxyl radical was derived exclusively from hydrogen peroxide and that there was no exchange of oxygen atoms between H2O2 and solvent water, and the complementary reaction with ordinary H2 O2 and 17O-labeled water also showed that none of the Hydroxylradical was derived from water.
TL;DR: In this paper, the use of dibenzothiophene with hydrogen peroxide using phosphotungstic acid as catalyst and tetraoctylammonium bromide as phase transfer agent in a mixture of water and toluene has been studied.
Abstract: Oxidation of dibenzothiophene with hydrogen peroxide using phosphotungstic acid as catalyst and tetraoctylammonium bromide as phase transfer agent in a mixture of water and toluene has been studied. Catalysed decomposition of hydrogen peroxide competes with dibenzothiophene oxidation but by choice of suitable conditions yields of dibenzothiophene sulphone approaching 100% may be obtained. Treatment of gas oils with this technology shows that all the sulphur compounds present are oxidised by this catalyst system and highly substituted dibenzothiophenes are the most readily oxidised of species containing a thiophene nucleus. Oxidised sulphur compounds can be separated from the oil by adsorption on silica gel. The use of oxidation and adsorption in a process for desulphurisation of gas oils is discussed.
TL;DR: The rate constants, k(r), are determined for scavenging .OH radicals by melatonin, 5-methoxytryptamine (5-MeO-T), 5-hydroxytryptamines (serotonin), 6-chloromelatonin (6-Cl-MLT, 6-hydroxymelatonin), and kynurenine (KN) in aqueous solutions.
TL;DR: A steady-state kinetic model describing the dependence of peroxidase activity on hydrogen peroxide concentration is presented and indicates that SBP tends to form more compound III and is catalytically slower than HRP during the oxidation of phenol.
TL;DR: The first instrumental method for simultaneous determination of peroxyacetic acid and hydrogen peroxide has been developed and external calibration with the solid standards of MTSO and TPPO leads to a very accurate and reliable method.
Abstract: The first instrumental method for simultaneous determination of peroxyacetic acid (PAA) and hydrogen peroxide has been developed. The successive quantitative reaction of PAA with methyl p-tolyl sulfide (MTS) and hydrogen peroxide with triphenylphosphine (TPP) yields the corresponding sulfoxide MTSO and phosphine oxide TPPO. The reagents and their oxides are separated by HPLC on reversed-phase columns with acetonitrile/water gradient elution within 5 min. External calibration with the solid standards of MTSO and TPPO leads to a very accurate and reliable method. Samples are stable and can be stored after derivatization for several days prior to analysis. Real samples from brewery disinfection were analyzed in comparison to titration with excellent correlation.
TL;DR: Generations of superoxide anions and hydrogen peroxide in the vascular tissue were particularly apparent in the xylem and associated with the sites of distribution of CuZn-SOD as determined by an immunohistochemical method, and also with the location of lignin as determined with the phloroglucin-HCl reaction.
Abstract: The sites of generations of superoxide anions and hydrogen peroxide in cross sections of hypocotyls from spinach seedlings were located by staining with nitroblue tetrazolium (NBT) and with starch-iodide, respectively. Formazan, produced upon the reduction of NBT by superoxide, was observed mainly in the vascular tissue only in the presence of inhibitors of CuZn-superoxide dismutase (CuZn-SOD), and its formation was suppressed under anaerobic conditions. Thus, NBT was reduced to formazan specifically by the superoxide anions generated in vascular tissue. The reduction of NBT was suppressed by inhibitors of NAD(P)H oxidase, but neither by cyanide nor azide, indicating the involvement of NAD(P)H oxidase in the generation of superoxide anions in the vascular tissue. Starch-I2 complex also was formed in the vascular tissue, but not in the presence of either the CuZn-SOD inhibitor or the NAD(P)H oxidase inhibitor, indicating that the hydrogen peroxide is produced via the catalytic disproportionation with CuZn-SOD of the superoxide generated by NAD(P)H oxidase. Generations of superoxide anions and hydrogen peroxide in the vascular tissue were particularly apparent in the xylem and associated with the sites of distribution of CuZn-SOD as determined by an immunohistochemical method, and also with the location of lignin as determined by the phloroglucin-HCl reaction.
TL;DR: The effects of the flavonoids quercetin and myricetin, and the antihepatotoxic agent silymarin, on hydrogen peroxide-mediated DNA damage in human lymphocytes were determined using alkaline single-cell gel electrophoresis (the comet assay).
Abstract: The effects of the flavonoids quercetin and myricetin, and the antihepatotoxic agent silymarin, on hydrogen peroxide-mediated DNA damage in human lymphocytes were determined using alkaline single-cell gel electrophoresis (the comet assay). Treatment with hydrogen peroxide increased the levels of DNA strand breaks and oxidised pyrimidine bases in these cells. Quercetin was protective at concentrations above 10 μM and myricetin decreased oxidant-induced DNA strand breakage at concentrations of 100 μM. Cellular metabolism may alter the antioxidant efficacy of the flavonoids. Silymarin had no protective effect at any of the concentrations tested. None of these flavonoids was itself genotoxic. Neither α-tocopherol nor β-carotene decreased hydrogen peroxide-induced DNA breakage. The differences in effectiveness of these dietary compounds against oxidative DNA damage may be explained by differences in their chemical structure or location within the cell.
TL;DR: It is suggested that the use of nanofiltration membranes for the recovery of phosphorous with a second type of technology is to be considered as a viable process for recovery of nitrogen in the short term.
TL;DR: The data indicate an almost exclusive role for catalase in the removal of H2O2 in normal human erythrocytes, as well as the different kinetics of these enzymes.
TL;DR: It is shown that, in the presence of hydrogen peroxide, 4-Aminobenzoic acid hydrazide irreversibly inactivates myeloperoxidase, and it is proposed that this inactivation is due to the oxidation of ABAH to a radical that reduces the enzyme to its ferrous intermediate.
Abstract: Hypochlorous acid is the most powerful oxidant generated by neutrophils and is likely to contribute to the damage mediated by these inflammatory cells. The haem enzyme myeloperoxidase catalyses its production from hydrogen peroxide and chloride. 4-Aminobenzoic acid hydrazide (ABAH) is a potent inhibitor of hypochlorous acid production. In this investigation we show that, in the presence of hydrogen peroxide, ABAH irreversibly inactivates myeloperoxidase. ABAH was oxidized by myeloperoxidase, and kinetic analysis of the inactivation conformed to that for a mechanism-based inhibitor. Inactivation was exacerbated by concentrations of hydrogen peroxide greater than 50 microM and by the absence of oxygen. Hydrogen peroxide alone caused minimal inactivation. Reduced glutathione inhibited the oxidation of ABAH as well as the irreversible inhibition of myeloperoxidase. In the presence of oxygen, ABAH and hydrogen peroxide initially converted myeloperoxidase into compound III, which subsequently lost haem absorbance. In the absence of oxygen, the enzyme was converted into ferrous myeloperoxidase and its haem groups were rapidly destroyed. We propose that myeloperoxidase oxidizes ABAH to a radical that reduces the enzyme to its ferrous intermediate. Ferrous myeloperoxidase reacts either with oxygen to allow enzyme turnover, or with hydrogen peroxide to give irreversible inactivation.
TL;DR: It is proposed that the peroxidase/phenolics/AA system can function as a hydrogen peroxide scavenging system and that in addition to AA, MDA radicals may also reduce phenoxyl radicals.
Abstract: The function of a peroxidase/phenolics/ascorbic acid system in plant vacuoles has not yet been well elucidated. We wished to study the redox reactions among hydrogen peroxide, phenolics and ascorbic acid (AA) in the presence of horseradish peroxidase. Horseradish peroxidase oxidized rutin and chlorogenic acid (CGA), compounds present in many kinds of plant. The oxidation was inhibited by AA. As a result of the inhibition, AA was oxidized and when almost all of it had been oxidized, oxidation of the phenolics commenced. Monodehydroascorbic acid (MDA) radical was detected during the oxidation of AA, suggesting that the inhibition of oxidation of rutin and CGA was due to reduction of phenoxyl radicals by AA. By comparison of time courses of changes in levels of AA and MDA radicals, and by kinetic calculation, it is suggested that in addition to AA, MDA radicals may also reduce phenoxyl radicals. It is proposed that the peroxidase/phenolics/AA system can function as a hydrogen peroxide scavenging system.
TL;DR: Results clearly identify Cys46 as the peroxidatic center of AhpC and Cys165 as an important residue for preserving the activity of wild-type AhPC by reacting with the nascent sulfenic acid of the oxidized protein (Cys46-SOH) to generate a stable disulfide bond, thus preventing further oxidation of Cys 46-S OH by substrate.
Abstract: The catalytic properties of cysteine residues Cys46 and Cys165, which form intersubunit disulfide bonds in the peroxidatic AhpC protein of the alkyl hydroperoxide reductase (AhpR) system from Salmonella typhimurium, have been investigated. The AhpR system, composed of AhpC and a flavoprotein reductase, AhpF, catalyzes the pyridine nucleotide-dependent reduction of organic hydroperoxides and hydrogen peroxide. Amino acid sequence analysis of the disulfide-containing tryptic peptide demonstrated the presence of two identical disulfide bonds per dimer of oxidized AhpC located between Cys46 on one subunit and Cys165 on the other. Mutant AhpC proteins containing only one (C46S and C165S) or no (C46,165S) cysteine residues were purified and shown by circular dichroism studies to exhibit no major disruptions in secondary structure. In NADH-dependent peroxidase assays in the presence of AhpF, the C165S mutant was fully active in comparison with wild-type AhpC, while C46S and C46,165S displayed no peroxidatic activity. In addition, only C165S was oxidized by 1 equiv of hydrogen peroxide, giving a species that was stoichiometrically reducible by NADH in the presence of a catalytic amount of AhpF. Oxidized C165S also reacted rapidly with a stoichiometric amount of the thiol-containing reagent 2-nitro-5-thiobenzoic acid to generate a mixed disulfide, and was susceptible to inactivation by hydrogen peroxide, strongly supporting its identification as a cysteine sulfenic acid (Cys46-SOH). The lack of reactivity of the C46S mutant toward peroxides was not a result of inaccessibility of the remaining thiol as demonstrated by its modification with 5, 5'-dithiobis(2-nitrobenzoic acid), but could be due to the lack of a proximal active-site base which would support catalysis through proton donation to the poor RO- leaving group. Our results clearly identify Cys46 as the peroxidatic center of AhpC and Cys165 as an important residue for preserving the activity of wild-type AhpC by reacting with the nascent sulfenic acid of the oxidized protein (Cys46-SOH) to generate a stable disulfide bond, thus preventing further oxidation of Cys46-SOH by substrate.
TL;DR: In this paper, a cellulose-based activated carbon cloth has been oxidized by air, nitric acid, hydrogen peroxide and iron nitrate cristallohydrate melt treatments.
TL;DR: Testing the hypothesis that vasodilator responses of cerebral arterioles to bradykinin involve activation of calcium-dependent potassium channels suggests activation of potassium channels may be a major mechanism of dilatation in response to reactive oxygen species in the cerebral microcirculation.
Abstract: Background and Purpose Relatively little is know regarding mechanisms by which reactive oxygen species produce dilatation of cerebral arterioles. The goal of this study was to test the hypothesis that vasodilator responses of cerebral arterioles to bradykinin, which produces endogenous generation of reactive oxygen species, involve activation of calcium-dependent potassium channels. Methods We used a cranial window in anesthetized rats to examine effects of catalase (which degrades hydrogen peroxide) on responses to bradykinin. In addition, we examined effects of tetraethylammonium (TEA) and iberiotoxin, inhibitors of calcium-dependent potassium channels, on responses of cerebral arterioles to hydrogen peroxide, bradykinin, and papaverine. Results In cerebral arterioles (baseline diameter=40±1 μm) (mean±SE), hydrogen peroxide (10 and 100 μmol/L) produced concentration-dependent dilatation. TEA (1 mmol/L), an inhibitor of calcium-dependent potassium channels, produced marked inhibition of vasodilatation in...
TL;DR: In this paper, the feasibility of a large scale application of the lightenhanced Fenton reaction has been investigated for the treatment of highly contaminated industrial waste water containing toxic aromatic amines (dimethyl anilines or xylidines) as the main pollutants.
Abstract: The feasibility of a large scale application of the light-enhanced Fenton reaction has been investigated for the treatment of a highly contaminated industrial waste water containing toxic aromatic amines (dimethyl anilines or xylidines) as the main pollutants. The Fenton reagent, a combination of hydrogen peroxide and a ferrous salt, is a potent oxidizing agent of organic compounds in acidic aqueous solution, and UV/visible irradiation may significantly enhance the degradation rates. Preliminary laboratory tests on the model compounds, 2,4- and 3,4-xylidine have been performed for selecting appropriate experimental conditions. Subsequent experimentation on the industrial waste water at a large scale level (3000 mg C l−1, 500 l) has been carried out using an experimental design methodology for the simulation and the evaluation of the effects of the two critical factors, hydrogen peroxide and ferrous ion concentrations. The results indicate that the light-enhanced Fenton reaction is a most effective treatment process under acidic conditions and is a realistic alternative to adsorption of xylidines on activated carbon as used at present.
TL;DR: A novel non-enzymatic pathway for NO synthesis involving hydrogen peroxide and D- or L-arginine and the addition of carboxy-2-phenyl-4, 4,5,5-tetramethyl-imidazoline-1-oxyl-3-oxide (PTIO) is demonstrated, confirming NO generation in the reaction.
TL;DR: In this article, the potential of the oxidation of various carcinogenic aromatic amines by Fenton's reagent [Fe(II) + H2O2] for liquid waste treatments was assessed.
TL;DR: The use of a catalytic amount of 3-cyanopyridine in the catalytic catalysts for terminal alkenes with aqueous hydrogen peroxide resulted in the formation of many functionalized epoxides in high yields.
TL;DR: A pseudo steady-state kinetic model of the HRP-hydrogen peroxide-aromatic compound system was modified to incorporate enzyme inactivation mechanisms in order to improve its predictive ability.
Abstract: Once activated by hydrogen peroxide, horseradish peroxidase (HRP) catalyzes the oxidation of aqueous aromatic compounds to produce high molecular weight polymers of low solubility. A pseudo steady-state kinetic model of the HRP-hydrogen peroxide-aromatic compound system was modified to incorporate enzyme inactivation mechanisms in order to improve its predictive ability. The kinetic constants of the model were calibrated using a series of experimental data sets. The model's ability to predict the time-dependent removal of phenol within the range of 0.5-6 mM from a batch reactor was validated. The model accounts for permanent losses of enzyme activity through inactivation by free radicals as well as interaction with end-product polymers as they form.