Showing papers on "Hydrogen peroxide published in 1996"
TL;DR: It is shown that in vivo generated macrophage foam cells produce superoxide, nitric oxide, and hydrogen peroxide after isolation from hypercholesterolemic rabbits and reactive oxygen species can modulate matrix degradation in areas of high oxidant stress and could therefore contribute to instability of atherosclerotic plaques.
Abstract: Vulnerable areas of atherosclerotic plaques often contain lipid-laden macrophages and display matrix metalloproteinase activity. We hypothesized that reactive oxygen species released by macrophage-derived foam cells could trigger activation of latent proforms of metalloproteinases in the vascular interstitium. We showed that in vivo generated macrophage foam cells produce superoxide, nitric oxide, and hydrogen peroxide after isolation from hypercholesterolemic rabbits. Effects of these reactive oxygens and that of peroxynitrite, likely to result from simultaneous production of nitric oxide and superoxide, were tested in vitro using metalloproteinases secreted by cultured human vascular smooth muscle cells. Enzymes in culture media or affinity-purified (pro-MMP-2 and MMP-9) were examined by SDS-PAGE zymography, Western blotting, and enzymatic assays. Under the conditions used, incubation with xanthine/xanthine oxidase increased the amount of active gelatinases, while nitric oxide donors had no noticeable effect. Incubation with peroxynitrite resulted in nitration of MMP-2 and endowed it with collagenolytic activity. Hydrogen peroxide treatment showed a catalase-reversible biphasic effect (gelatinase activation at concentrations of 4 microM, inhibition at > or = 10-50 microM). Thus, reactive oxygen species can modulate matrix degradation in areas of high oxidant stress and could therefore contribute to instability of atherosclerotic plaques.
1,117 citations
TL;DR: Questions concerning the involvement of free hydroxyl radicals or reactions of metal/oxo intermediates may obscure a wider appreciation of the importance of Fenton chemistry involving hypohalous acids rather than hydrogen peroxide as the oxidant.
Abstract: In 1876, Fenton described a colored product obtained on mixing tartaric acid with hydrogen peroxide and a low concentration of a ferrous salt. Full papers in 1894 and 1896 showed the product was dihydroxymaleic acid. Haber, Weiss and Willstatter proposed in 1932-1934 the involvement of free hydroxyl radicals in the iron(II)/hydrogen peroxide system, and Baxendale and colleagues around 1950 suggested that superoxide reduces the iron(III) formed on reaction, explaining the catalytic nature of the metal. Since Fridovich and colleagues discovered the importance of superoxide dismutase in 1968, numerous studies have sought to explain the deleterious effects of cellular oxidative stress in terms of superoxide-driven Fenton chemistry. There remain questions concerning the involvement of free hydroxyl radicals or reactions of metal/oxo intermediates. However, these outstanding questions may obscure a wider appreciation of the importance of Fenton chemistry involving hypohalous acids rather than hydrogen peroxide as the oxidant.
528 citations
TL;DR: In this paper, the peroxidase-modified amperometric electrodes have been widely studied and developed, not only because of hydrogen and organic peroxides are important analytes but also because of the key role of hydrogen peroxide detection in coupled enzyme systems, in which the peroxide is formed as the product of the enzymatic reaction.
494 citations
TL;DR: In the absence of iron, equimolar fluxes of NO and O interact to yield potent oxidants such as ONOO/ONOOH, which oxidize organic compounds.
358 citations
TL;DR: In this article, the role of Fenton's reaction [oxidation of Fe(II) by hydrogen peroxide] in the catalytic cycle was examined, and a number of competing processes were observed in model systems.
Abstract: Iron redox cycling can catalyze the oxidation of humic substances and increase the rate of oxygen consumption in surface waters rich in iron and organic carbon. This study examines the role of Fenton`s reaction [oxidation of Fe(II) by hydrogen peroxide] in this catalytic cycle. A number of competing processes were observed in model systems containing dissolved Fe, hydrogen peroxide, and Suwannee River fulvic acid. First, the effective rate constant of Fenton`s reaction increased with increasing fulvic acid concentration, indicating the formation Fe(II)-fulvate complexes that react more rapidly with hydrogen peroxide than Fe(II)-aquo complexes. This effect was significant at pH 5 but negligible at pH 3. A second effect was scavenging of the HO{sup .} radical produced in Fenton`s reaction by fulvic acid, forming an organic radical. The organic radical reduced oxygen to HO{sub 2}{sup .}/O{sub 2}{sup .-}, which then regenerated hydrogen peroxide by reaction with Fe(II). Finally, Fe(III) was reduced by a dark reaction with fulvic acid, characterized by an initially fast reduction followed by slower processes. The behavior of Fe(II) and hydrogen peroxide over time in the presence of fulvic acid and oxygen could be described by a kinetic model taking all of these reactions into account. The netmore » result was an iron redox cycle in which hydrogen peroxide as well as oxygen were consumed (even though direct oxidation of Fe(II) by oxygen was not significant), and the oxidation of fulvic acid was accelerated. 56 refs., 7 figs., 1 tab.« less
354 citations
TL;DR: In this paper, the degradation of chemical compounds by acoustic cavitation is shown to involve three distinct pathways: 1) oxidation by hydroxyl radicals, 2) pyrolytic decomposition and 3) supercritical water oxidation.
325 citations
TL;DR: Pharmacological evidence is provided that hydrogen peroxide and peroxynitrite reversibly dilate cerebral arterioles by activating ATP-sensitive potassium channels, probably through an oxidant mechanism, whereas superoxide dilates cerebral arteriolaes by opening calcium-activated potassium channels.
Abstract: We investigated the role of potassium channels in the vasodilator action of hydrogen peroxide, peroxynitrite, and superoxide on cerebral arterioles. We studied the effect of topical application of these agents in anesthetized cats equipped with cranial windows. Hydrogen peroxide and peroxynitrite induced dose-dependent dilation that was inhibited by glyburide, an inhibitor of ATP-sensitive potassium channels. Superoxide, generated by xanthine oxidase acting on xanthine in the presence of catalase, also induced dose-dependent dilation of cerebral arterioles that was unaffected by glyburide but inhibited completely by tetraethylammonium chloride, an inhibitor of calcium-activated potassium channels. The vasodilations from hydrogen peroxide, peroxynitrite, or superoxide were unaffected by inhibition of soluble guanylate cyclase with LY-83583. The findings provide pharmacological evidence that hydrogen peroxide and peroxynitrite reversibly dilate cerebral arterioles by activating ATP-sensitive potassium channels, probably through an oxidant mechanism, whereas superoxide dilates cerebral arterioles by opening calcium-activated potassium channels. Activation of soluble guanylate cyclase is not a mediator of the vasodilator action of these agents in cerebral arterioles.
302 citations
TL;DR: A series of oxoperoxovanadium(V) complexes were characterized as functional models for the vanadium haloperoxidase enzymes as mentioned in this paper, and the crystal structures of these complexes were obtained.
Abstract: A series of oxoperoxovanadium(V) complexes (ligands: H3nta = nitrilotriacetic acid, H3heida = N-(2-hydroxyethyl)iminodiacetic acid, H2ada = N-(2-amidomethyl)iminodiacetic acid, Hbpg = N,N-bis(2-pyridylmethyl)glycine, and tpa = N,N,N-tris(2-pyridylmethyl)amine) were characterized as functional models for the vanadium haloperoxidase enzymes. The crystal structures of K[VO(O2)Hheida], K[VO(O2)ada], [VO(O2)bpg], and H[VO(O2)bpg]2(ClO4) were obtained. These complexes all possess a distorted pentagonal bipyramidal coordination sphere containing a side-on bound peroxide. In the presence of sufficient acid equivalents these complexes catalyze the two-electron oxidation of bromide or iodide by peroxide. Halogenation of an organic substrate was demonstrated by following the visible conversion of Phenol Red to Bromophenol Blue. In the absence of substrate, dioxygen can be generated by the halide-assisted disproportionation of hydrogen peroxide. In addition, some of these complexes can efficiently catalyze the perox...
296 citations
TL;DR: An amperometric enzyme electrode for hydrogen peroxide was developed via easy and effective enzyme immobilization using the sol-gel technique in this article, which comprises horseradish peroxidase (HRP) immobilized in the silica solgel matrix on a carbon paste electrode.
286 citations
TL;DR: It is proposed that O=N-OOCO 2- rearranges to give a nitrocarbonate anion, O2N-OCO2- which in turn, may serve as the proximal oxidant in biological systems that produce peroxynitrite.
280 citations
TL;DR: The present results raise the possibility that the major function of glutathione peroxidase may be the disposal of organic peroxides rather than the removal of hydrogen peroxide.
TL;DR: It is demonstrated that micromolar concentrations of 3-HK cause cell death in primary neuronal cultures prepared from rat striatum, suggesting that this endogenous compound should be regarded as an important factor in pathogenesis of neurodegenerative disorders.
Abstract: 3-Hydroxykynurenine (3-HK) is a tryptophan metabolite whose level in the brain is markedly elevated under several pathological conditions, including Huntington disease and human immunodeficiency virus infection. Here we demonstrate that micromolar concentrations (1-100 microM) of 3-HK cause cell death in primary neuronal cultures prepared from rat striatum. The neurotoxicity of 3-HK was blocked by catalase and desferrioxamine but not by superoxide dismutase, indicating that the generation of hydrogen peroxide and hydroxyl radical is involved in the toxicity. Measurement of peroxide levels revealed that 3-HK caused intracellular accumulation of peroxide, which was largely attenuated by application of catalase. The peroxide accumulation and cell death caused by 1-10 microM 3-HK were also blocked by pretreatment with allopurinol or oxypurinol, suggesting that endogenous xanthine oxidase activity is involved in exacerbation of 3-HK neurotoxicity. Furthermore, NADPH diaphorase-containing neurons were spared from toxicity of these concentrations of 3-HK, a finding reminiscent of the pathological characteristics of several neurodegenerative disorders such as Huntington disease. These results suggest that 3-HK at pathologically relevant concentrations renders neuronal cells subject to oxidative stress leading to cell death, and therefore that this endogenous compound should be regarded as an important factor in pathogenesis of neurodegenerative disorders.
TL;DR: In this paper, the influence of the nature of solvent on the reactivity and selectivity features of the large pore Ti-beta catalyst has been studied during the oxidation of 1-hexene and cyclohexanol, as representative substrates, using aqueous hydrogen peroxide as oxidant and under single liquid phase conditions.
TL;DR: Steady-state and total body oxidative damage to these targets can now be approximated, providing a tool to examine the effects of “antioxidants” in vivo.
Abstract: Publisher Summary Words such as “antioxidant” and “oxidative stress” are difficult to define. The term “antioxidant” used in the literature is restricted to chain-breaking antioxidant inhibitors of lipid peroxidation. Food scientists frequently equate antioxidants to inhibitors of lipid peroxidation because they use antioxidants to prevent rancidity. Free radicals generated in vivo damage proteins, DNA, and other molecules in addition to lipids. A broader definition is: an antioxidant is any substance that when present at low concentrations compared to those of an oxidizable substrate delays or prevents oxidation of that substrate. Mechanisms of antioxidant action can include: removal of O 2 , scavenging reactive oxygen/nitrogen species or their inhibiting ROS/RNS formation, binding metal ions needed for catalysis of ROS generation, and up regulation of endogenous antioxidant defenses. This chapter emphasizes the importance of the source of stress and the target (“oxidizable substrate”) measured; but also mentions the cases that the definition does not include. When ROS/RNS are generated in vivo , many antioxidants come into play. The chapter discusses the antioxidants known, or proposed, to be important in aerobic organisms. There is outline on some approaches to the characterization of direct antioxidant activity and discussion on biologically relevant ROS/RNS—superoxide and hydrogen peroxide, hydroxyl radical, peroxyl radicals, lipid peroxidation, hypochlorous acid, heme proteins/peroxides, peroxynitrite, and singlet oxygen—measuring their scavenging, their reactions, some inhibitions on radical formation and other properties. Some approaches have been listed to help prove that a given compound act as an antioxidant in vivo , including two approaches for putative antioxidants. Specific assays are being developed to measure rates of oxidative damage to protein, DNA, and lipid. Steady-state and total body oxidative damage to these targets can now be approximated, providing a tool to examine the effects of “antioxidants” in vivo .
TL;DR: In this paper, a model for the deposition of cerium-rich films on copper under cathodic polarization was studied as a model system for understanding the mechanism of corrosion inhibition of copper-containing aluminum alloys.
Abstract: The deposition of cerium-rich films on copper under cathodic polarization was studied as a model system for understanding the mechanism of corrosion inhibition of copper-containing aluminum alloys. Deposition was also studied on gold and iron for comparison with copper. Inhibition of corrosion of the aluminum alloys is achieved by deposition of a cerium-rich film on the copper-containing intermetallics that blocks the cathodic reduction of oxygen at these sites. X-ray absorption near-edge structure measurements show that cerium-rich films precipitated from aerated solutions are in the tetravalent state. Thermodynamically, the Pourbaix diagram predicts that under these conditions cerium should be in the trivalent state. This indicates that cerium chemistry is determined by processes in the solution rather than the potential of the electrode. Cerium-rich film formation is dependent on reduction of oxygen which influences the oxidation of Ce(III) to Ce(IV) in solution and precipitation of the film by changing the local pH at the electrode. The generation of hydrogen peroxide by oxygen reduction is considered to enhance cerium-rich film formation by oxidizing Ce(III) to Ce(IV) in solution. This was confirmed by addition of hydrogen peroxide to the solution.
TL;DR: In this paper, the degradation of acetone was carried out in a UV reactor in the presence of ∼16 mM H2O2 such that most of the UV was absorbed by H 2O2.
Abstract: Acetone is a significant pollutant in contaminated groundwaters and industrial effluents. It can be treated by the UV/H2O2 process but only slowly. This study aims to understand the degradation mechanism and hence the reasons for slow treatment. The degradation of acetone was carried out in a UV reactor in the presence of ∼16 mM H2O2 such that most of the UV was absorbed by H2O2. The decay of acetone was followed by gas chromatography, and the generation of intermediates (identified as acetic, formic, and oxalic acids) was followed by ion chromatography. Measurement of the total organic carbon indicated a complete carbon balance throughout the reaction ending in mineralization. A kinetic model, based on an assumed mechanism, was developed that generated a profile of reactants and intermediates in agreement with the experimental data, including the pH profile. The initial concentrations of acetone and hydrogen peroxide strongly affect the initial rate of acetone degradation, but no pH effect was observed i...
01 Jan 1996
TL;DR: The fur mutants, which have an intracellular iron overload, were more sensitive to HOCl, supporting the generation of hydroxyl radicals upon HOCl exposure via a Fenton-type reaction.
Abstract: We have investigated the mechanisms of killing of Escherichia coli by HOCl by identifying protective functions. HOCl challenges were performed on cultures arrested in stationary phase and in exponential phase. Resistance to HOCl in both cases was largely mediated by genes involved in resistance to hydrogen peroxide (H2O2). In stationary phase, a mutation in rpoS, which controls the expression of starvation genes including those which protect against oxidative stress, renders the cells hypersensitive to killing by HOCl. RpoS-regulated genes responsible for this sensitivity were dps, which encodes a DNA-binding protein, and, to a lesser extent, katE and katG, encoding catalases; all three are involved in resistance to H2O2. In exponential phase, induction of the oxyR regulon, an adaptive response to H2O2, protected against HOCl exposure, and the oxyR2 constitutive mutant is more resistant than the wild-type strain. The genes involved in this oxyR-dependent resistance have not yet been identified, but they differ from those primarily involved in resistance to H2O2, including katG, ahp, and dps. Pretreatment with HOCl conferred resistance to H2O2 in an OxyR-independent manner, suggesting a specific adaptive response to HOCl. fur mutants, which have an intracellular iron overload, were more sensitive to HOCl, supporting the generation of hydroxyl radicals upon HOCl exposure via a Fenton-type reaction. Mutations in recombinational repair genes (recA or recB) increased sensitivity to HOCl, indicative of DNA strand breaks. Sensitivity was visible in the wild type only at concentrations above 0.6 mg/liter, but it was observed at much lower concentrations in dps recA mutants.
TL;DR: In this article, the photocatalytic degradation of two environmentally relevant organic compounds [4-chlorophenol (4-CP) and p-toluenesulfonic acid (PTSA)] was investigated using a novel cylindrical fluidized bed photoreactor (FBPR).
Abstract: The photocatalytic degradation of two environmentally relevant organic compounds [4-chlorophenol (4-CP) and p-toluenesulfonic acid (PTSA)] was investigated using a novel cylindrical fluidized bed photoreactor (FBPR). Accumulated biodegradable organic acids, identified as intermediate reaction products, decreased after the removal of original pollutants. Measurements of the oxygen uptake rates with a mixed culture showed that all intermediate photooxidation products were much better biodegradable than the initial aromatic pollutants (4-CP, PTSA). The influence of HCO3- and Cl- on the degradation rate was also studied. For concentrations of 1 mM bicarbonate (HO• radical scavenger) and of 140 mM chloride (photoinhibitor), the photocatalytic degradation rate decreased by 50%. During the photocatalytic reaction process, hydrogen peroxide accumulated in solution up to 0.21 mM depending on the initial concentration of the organic compounds and the concentration of dissolved oxygen. The relative quantum efficienc...
TL;DR: The peroxynitrite in these postprocessed solutions has a broad absorption spectrum with a maximum around 302 nm, follows a characteristic first-order decomposition at pH 7.2 and 25°C, and reacts with organic compounds to give either nitrated or one-electron transfer products.
TL;DR: It is demonstrated that NO possesses properties which protect against ROS toxicity and how the use of different NO donor compounds can lead to different conclusions about the role that NO can play in the cytotoxicity of ROS is demonstrated.
TL;DR: Some possible antimicrobial uses of H2O2 in the food industry are presented and its capacity-generally mediated by transition metal ions-to generate more reactive and cytotoxic oxygen species such as the hydroxyl radical is reported.
Journal Article•
TL;DR: It is concluded that monocyte-derived reactive oxygen metabolites kill NK cells by apoptosis and that NK cells are unusually sensitive to oxidatively as well as non-oxidatively induced apoptosis.
Abstract: Human NK cells (with CD3-/56+ phenotype) acquired features characteristic of apoptosis after incubation with autologous monocytes, as revealed by apoptotic nuclear morphology, degradation of DNA into oligonucleosomal fragments, and reduced nuclear interchalation of propidium iodide. In contrast, T cells (CD3+/56-) remained non-apoptotic. The monocyte-induced apoptosis in NK cells was prevented by catalase, a scavenger of hydrogen peroxide; whereas superoxide dismutase (a scavenger of superoxide anion), hydroxyl radical scavengers such as mannitol and deferoxamine, or the hypochlorus acid scavenger taurine did not prevent apoptosis. Sodium azide, a myeloperoxidase inhibitor, substantially reduced the monocyte-induced apoptosis in NK cells. Exogenous hydrogen peroxide, at concentrations exceeding 1 microns, induced apoptosis in both NK and T cells. Apoptosis induced by hydrogen peroxide occurred independently of synthesis of protein or mRNA and was blocked by the endonuclease inhibitor aurin tricarboxylic acid. Furthermore, oxidatively induced apoptosis in NK cells was inhibited by herbimycin A, indicating that apoptosis was dependent on protein kinases. Two to five times more hydrogen peroxide was required to induce apoptosis in T cells compared with NK cells. Similarly, NK cells were considerably more susceptible to apoptosis induced by the topoisomerase II inhibitor etoposide or by gamma-irradiation than were T cells. We conclude that monocyte-derived reactive oxygen metabolites kill NK cells by apoptosis and that NK cells are unusually sensitive to oxidatively as well as non-oxidatively induced apoptosis.
TL;DR: In this article, the treatment of a diesel-contaminated soil with hydrogen peroxide catalyzed by six iron compounds and by naturally-occurring minerals in which the pH is stabilized by phosphate was investigated using central composite rotatable experimental designs.
TL;DR: A plasmid containing a transcriptional fusion of the Escherichia coli katG promoter to a truncated Vibrio fischeri lux operon (luxCDABE) was constructed in this paper.
Abstract: A plasmid containing a transcriptional fusion of the Escherichia coli katG promoter to a truncated Vibrio fischeri lux operon (luxCDABE) was constructed. An E. coli strain bearing this plasmid (strain DPD2511) exhibited low basal levels of luminescence, which increased up to 1,000-fold in the presence of hydrogen peroxide, organic peroxides, redox-cycling agents (methyl viologen and menadione), a hydrogen peroxide-producing enzyme system (xanthine and xanthine oxidase), and cigarette smoke. An oxyR deletion abolished hydrogen peroxide-dependent induction, confirming that oxyR controlled katG'::lux luminescence. Light emission was also induced by ethanol by an unexplained mechanism. A marked synergistic response was observed when cells were exposed to both ethanol and hydrogen peroxide; the level of luminescence measured in the presence of both inducers was much higher than the sum of the level of luminescence observed with ethanol and the level of luminescence observed with hydrogen peroxide. It is suggested that this construction or similar constructions may be used as a tool for assaying oxidant and antioxidant properties of chemicals, as a biosensor for environmental monitoring and as a tool for studying cellular responses to oxidative hazards.
Journal Article•
TL;DR: Comparison to the untreated control surfaces revealed that enamel exposed to the bleaching agents underwent slight morphologic surface alterations, while the enamel surfaces treated with phosphoric acid showed severe morphologic alterations.
Abstract: The effects of four bleaching agents (Opalescence, HiLite, 30% hydrogen peroxide, and 30% hydrogen peroxide mixed with sodium perborate) and 37% phosphoric acid on the external surface of human enamel were examined with the scanning electron microscope. The materials were applied to the enamel surfaces of 60 specimens obtained from 10 teeth. Each test agent was applied to one specimen from each tooth. One specimen of each tooth was left untreated. Comparison to the untreated control surfaces revealed that enamel exposed to the bleaching agents underwent slight morphologic surface alterations. The enamel surfaces treated with phosphoric acid, in contrast, showed severe morphologic alterations.
TL;DR: Assay results provide the first direct evidence for a catalytic mechanism for peroxide reduction involving redox-active disulfides within each protein in Salmonella typhimurium.
Abstract: The two components, AhpF and AhpC, of the Salmonella typhimurium alkyl hydroperoxide reductase enzyme system have been overexpressed and purified from Escherichia coli for investigations of their catalytic properties. Recombinant proteins were isolated in high yield (25−33 mg per liter of bacterial culture) and were shown to impart a high degree of protection against killing by cumene hydroperoxide to the host E. coli cells. We have developed quantitative enzymatic assays for AhpF alone and for the combined AhpF/AhpC system which have allowed us to address such issues as substrate specificity and inhibition by thiol reagents for each protein. All assays gave identical results whether overexpressed S. typhimurium proteins from E. coli or proteins isolated directly from S. typhimurium were used. Anaerobic hydroperoxide reductase assays have demonstrated that cumene hydroperoxide, ethyl hydroperoxide, and hydrogen peroxide can all be reduced by the combined enzyme system. AhpF possesses multiple pyridine nuc...
TL;DR: The reactivities of various antioxidative compounds including catechol derivatives and endogenous radical scavengers toward hydroxyl radical (.OH) were investigated by an electron spin resonance-spin trapping method, thiobarbituric acid method, and DNA strand scission assay.
TL;DR: There were no significant differences among treatments in percent hatch or final infection for uninfected eggs receiving prophylactic chemical treatments, but the compound was less effective at inhibiting fungal growths compared with hydrogen peroxide and formalin treatments.
TL;DR: Ascorbate‐dependent detoxification of hydrogen peroxide by guaiacol‐type peroxidases is increased considerably in the presence of 3,4‐dihydroxyphenolic compounds, suggesting that ascorbate is the natural substrate for many types of peroxIDase in situ and not just the asCorbate‐specific peroxideases.