Showing papers on "Hydrogen peroxide published in 1986"
TL;DR: It was found that homocysteine plus copper could lyse the cells in a dose-dependent manner, an effect that was completely prevented by catalase, and these findings may be relevant to the mechanism of some types of chronic vascular injury.
Abstract: We have examined whether the toxic effects of homocysteine on cultured endothelial cells could result from the formation and action of hydrogen peroxide. In initial experiments with a cell-free system, micromolar amounts of copper were found to catalyze an oxygen-dependent oxidation of homocysteine. The molar ratio of homocysteine oxidized to oxygen consumed was approximately 4.0, which suggests that oxygen was reduced to water. The addition of catalase, however, decreased oxygen consumption by nearly one-half, which suggests that H2O2 was formed during the reaction. Confirming this hypothesis, H2O2 formation was detected using the horseradish peroxidase-dependent oxidation of fluorescent scopoletin. Ceruloplasmin was also found to catalyze oxidation of homocysteine and generation of H2O2 in molar amounts equivalent to copper sulfate. Finally, homocysteine oxidation was catalyzed by normal human serum in a concentration-dependent manner. Using cultured human and bovine endothelial cells, we found that homocysteine plus copper could lyse the cells in a dose-dependent manner, an effect that was completely prevented by catalase. Homocystine plus copper was not toxic to the cells. Specific injury to endothelial cells was seen only after 4 h of incubation with homocysteine plus copper. Confirming the biochemical studies, ceruloplasmin was also found to be equivalent to Cu++ in its ability to cause injury to endothelial cells in the presence of homocysteine. Since elevated levels of homocysteine have been implicated in premature development of atherosclerosis, these findings may be relevant to the mechanism of some types of chronic vascular injury.
834 citations
TL;DR: Hydroxyl radical Lipid peroxidation Transferrin iron binding Heme‐protein iron release Hemoglobin Fenton catalyst Desferrioxamine Bleomycin‐detectable iron.
626 citations
TL;DR: In this article, rate laws for the aqueous oxidation of pyrite by ferric ion, dissolved oxygen and hydrogen peroxide at 30°C in dilute, acidic chloride solutions were derived.
524 citations
TL;DR: The experiments suggest that injury to cardiac mitochondria which is produced by anthracycline antibiotics may result from the generation of the hydroxyl radical during anthrACYcline metabolism by NADH dehydrogenase.
483 citations
TL;DR: In this article, the authors propose a method for the Oxydation de cinnamaldehydes, benzaldehyde, furfural, pyridine carbaldehyde-4, thiophene carbaldehyde, 2 pyrrolecarbaldehyde-2, alcenals, dans l'acetonitrile et dans different solvants alcooliques.
Abstract: Oxydation de cinnamaldehydes, benzaldehydes, furfural, pyridinecarbaldehyde-4, thiophenecarbaldehyde-2, pyrrolecarbaldehyde-2, alcenals, dans l'acetonitrile et dans differents solvants alcooliques
460 citations
TL;DR: Hydrogen peroxide treatment induces the synthesis of 30 proteins in Salmonella typhimurium, including the highly conserved DnaK protein, which is shown to be largely different from those proteins induced by aerobiosis.
Abstract: Hydrogen peroxide treatment induces the synthesis of 30 proteins in Salmonella typhimurium. Five of these proteins are also induced by heat shock, including the highly conserved DnaK protein. The induction of one of these five proteins by heat shock is dependent on oxyR, a positive regulator of hydrogen peroxide-inducible genes, while the induction of the other four by heat shock is oxyR independent. Five of the 30 hydrogen peroxide-inducible proteins have been identified, and their structural genes have been mapped. Other stresses such as nalidixic acid, ethanol, or cumene hydroperoxide treatment also induce subsets of the 30 hydrogen peroxide-inducible proteins as well as additional proteins. Hydrogen peroxide-inducible proteins are shown to be largely different from those proteins induced by aerobiosis. In addition, the expression of the katG (catalase) gene is shown to be regulated by oxyR at the level of mRNA.
460 citations
TL;DR: Two representative, hydrogen peroxide-dependent extracellular enzymes produced by ligninolytic cultures of the white-rot fungus Phanerochaete chrysosporium BKM-F-1767, were purified and their properties compared.
358 citations
TL;DR: This chapter discusses the preparation and characterization of chloramines, which represent an important class of leukocyte oxidants and contribute to oxidative microbicidal, cytotoxic and cytolytic activities, the chemical modification of regulatory substances, and the uptake and metabolism of nitrogen compounds.
Abstract: Publisher Summary This chapter discusses the preparation and characterization of chloramines. Chloramines represent an important class of leukocyte oxidants and contribute to oxidative microbicidal, cytotoxic and cytolytic activities, the chemical modification of regulatory substances, and the uptake and metabolism of nitrogen compounds. These are products of the reaction of hypochlorous acid (HOCl) or other chlorinating agents with primary and secondary amines. The production of HOCl by leukocytes is the result of peroxidase-catalyzed oxidation of chloride (Cl – ) by hydrogen peroxide (H 2 O 2 ). HOCl is in equilibrium with hypochlorite (OCl – ) and chlorine (Cl 2 ). The most abundant N-moieties available for reaction with HOCl in biological systems are primary amino groups, such as taurine, polyamines, amino sugars, lysine residues, and protein amino termini. Leukocyte peroxidases catalyze the oxidation of bromide (Br – ), iodide (I – ), thiocyanate (SCN – ), and Cl – . N–Cl derivatives are used within minutes of preparation to avoid decomposition or rearrangement. However, most are stable at 4° for hours or days at the appropriate pH.
345 citations
TL;DR: In this article, a chemical mechanism for the gas phase atmospheric oxidation of NOx and sulfur dioxide (SO2) in the presence of reactive hydrocarbons (RHC) has been developed for use in long-range transport modeling.
Abstract: A chemical mechanism for the gas phase atmospheric oxidation of nitrogen oxides (NOx) and sulfur dioxide (SO2) in the presence of reactive hydrocarbons (RHC) has been developed for use in long-range transport modeling. The mechanism includes numerous reactions important for nighttime and multiday simulations which have been previously ignored in photochemical mechanisms designed for urban scale applications. This mechanism is capable of simulating the decay of NOx/SO2/RHC precursors and the formation of oxidation products such as nitric acid, sulfuric acid, ozone, hydrogen peroxide, hydroperoxides, and organic peroxides which have recognized roles in the acidification of precipitation. Testing of detailed and condensed versions of the chemical mechanism is reported.
338 citations
TL;DR: Findings support the hypothesis that neutrophil activation and oxidant production are involved in the pathogenesis of ARDS.
331 citations
TL;DR: Results indicate that sodium chromate(VI) reacts with hydrogen peroxide to form tetraperoxochromate(V), leading to the production of the hydroxyl radical, which causes every base alteration and deoxyribose-phosphate backbone breakage.
TL;DR: Results suggest that drug-induced hydrogen peroxide and hydroxyl radical production may play a role in the antineoplastic action of redox active anticancer quinones.
Abstract: The cytotoxicity of the clinically important antineoplastic quinones doxorubicin, mitomycin C, and diaziridinylbenzoquinone for the Ehrlich ascites carcinoma was significantly reduced or abolished by the antioxidant enzymes catalase and superoxide dismutase, the hydroxyl radical scavengers dimethyl sulfoxide, diethylurea, and thiourea, and the iron chelators deferoxamine, 2,2-bipyridine, and diethylenetriaminepentaacetic acid. However, tumor cell killing by 5-iminodaunorubicin, a doxorubicin analog with a modified quinone function that prohibits oxidation-reduction cycling, was not ameliorated by any of the free radical scavengers tested. Furthermore, treatment of intact tumor cells with doxorubicin, mitomycin C, and diaziridinylbenzoquinone but not 5-iminodaunorubicin generated the hydroxyl radical, or a related chemical oxidant, in vitro in a process that required hydrogen peroxide, iron, and intact tumor cells. These results suggest that drug-induced hydrogen peroxide and hydroxyl radical production may play a role in the antineoplastic action of redox active anticancer quinones.
TL;DR: Even though NAC is very effective in protecting cells of different origins from the toxicity of reactive components in tobacco smoke and reactive oxygen species, a direct scavenging effect by NAC in vivo, particularly when administered orally, does not seem likely.
Abstract: N-acetylcysteine (NAC) is a thiol-containing compound which nonenzymatically interacts and detoxifies reactive electrophiles and free radicals. NAC was shown to effectively protect human bronchial fibroblasts against the toxic effects of tobacco smoke condensates and the isolated perfused lung against the glutathione (GSH)-depleting effect of tobacco smoke. NAC was also shown to reduce the reactive oxygen intermediate hydrogen peroxide (H2O2) and protect against the toxic effects of H2O2. In vivo studies, however, demonstrated that NAC when administered orally has very low bioavailability due to rapid metabolism to GSH among other metabolites. Thus, even though NAC is very effective in protecting cells of different origins from the toxicity of reactive components in tobacco smoke and reactive oxygen species, a direct scavenging effect by NAC in vivo, particularly when administered orally, does not seem likely. The bioavailability of NAC itself is very low when given this route. A more relevant mechanism in vivo for any protective effect NAC may exert against toxic species may be due to NAC acting as a precursor of GSH and facilitating its biosynthesis. GSH will then serve as the protective agent and detoxify reactive species both enzymatically and nonenzymatically.
Patent•
20 Jun 1986
TL;DR: A sterilization process where articles contacted with hydrogen peroxide are subjected to plasma treatment to generate an active species from the residual peroxide which effects sterilization of the article and concurrently removes the residual hydrogen peroxides by converting it into non-toxic decomposition products is described in this article.
Abstract: A sterilization process wherein articles contacted with hydrogen peroxide and containing trace amounts of residual hydrogen peroxide are subjected to plasma treatment to generate an active species from the residual hydrogen peroxide which effects sterilization of the article and concurrently removes the residual hydrogen peroxide by converting it into non-toxic decomposition products.
TL;DR: This chapter describes three assays for the quantitation of the cyanide resistant oxidative metabolism of macrophages, measuring O 2 – and H 2 O 2 production and nitroblue tetrazolium (NBT) reduction by cells cultured in 96-well microplates with the aid of an enzyme immunoassay microplate reader fitted with appropriate filters for the photometric determination of the respective reaction products.
Abstract: Publisher Summary This chapter describes three assays for the quantitation of the cyanide resistant oxidative metabolism of macrophages. Macrophages of various tissue origins produce copious amounts of superoxide (O 2 – ) and hydrogen peroxide (H 2 O 2 ) when adequately stimulated. This process is accompanied by a marked increment in oxygen uptake and an increased utilization of glucose via the hexose monophosphate shunt (HMPS). The coordinated sequence of reactions is known as the “oxidative” or “respiratory” burst. The three methods have in common the measurement of O 2 – and H 2 O 2 production and nitroblue tetrazolium (NBT) reduction by cells cultured in 96-well microplates with the aid of an enzyme immunoassay microplate reader fitted with appropriate filters for the photometric determination of the respective reaction products. The microassay of O 2 – production is based on the reduction of ferricytochrome c by O 2 – , the specificity of reduction being controlled by its inhibition by superoxide dismutase. The length of time for which O 2 – production occurs at a linear rate depends on the type of macrophage, on the cell density, and on the nature of the stimulus.
TL;DR: The discovery of the enzyme superoxide dismutase that catalyzed the production of hydrogen peroxide from superoxide anion defined the new field of oxygen metabolism in biologic systems and a potential role of oxidation/reduction reactions in both physiologic and pathologic conditions.
TL;DR: In this article, the temperature dependence of the Henry's law constant is expressed by KH = e[A/T−B], where KH is in the units of molar concentration per atm, and T is in degrees Kelvin.
Abstract: The Henry's law constants for aqueous solutions of hydrogen peroxide, methylhydroperoxide, and peroxyacetic acid were measured over the temperature range 278°–293°K. These determinations were made by measuring the vapor pressure of the peroxide in a gas stream of nitrogen or air that was in equilibrium with a solution of known peroxide concentration. The aqueous phase concentrations ranged from 5 × 10−5 M to 5 × 10−3 M for hydrogen peroxide, and from 1 × 10−6 M to 1 × 10−4 M for methylhydroperoxide and peroxyacetic acid. In all cases, Henry's law was obeyed over the concentration range investigated. The temperature dependence of the Henry's law constant is expressed by KH = e[A/T−B], where KH is in the units of molar concentration per atm, and T is in degrees Kelvin. The coefficients' values are A = 6621, B = 11.00 for hydrogen peroxide; A = 5607, B = 13.41 for methylhydroperoxide; and A = 6171, B = 14.55 for peroxyacetic acid. The experimental errors on KH at the 95% confidence level are ±8.3% for hydrogen peroxide, ±11% for methylhydroperoxide, and ±17% for peroxyacetic acid. In addition, the Henry's law behavior of hydrogen peroxide in aqueous solutions of sulfuric acid and ammonium sulfate was investigated. The Henry's law constant of hydrogen peroxide decreased with increasing sulfuric acid concentration and increased with increasing ammonium sulfate concentration.
TL;DR: The reaction between hydrogen peroxide and ferrous EDTA generates an oxidizing intermediate (I1) which is not the hydroxyl radical but shows a pattern of reactivity more associated with a metal ion oxidant like a ferryl (FeO2+)-EDTA complex.
TL;DR: The main blood constituents which could interfere in clinical glucose measurements using a hydrogen peroxide based glucose electrode have been investigated using several different membranes and constant and sweeping potentials.
TL;DR: The reaction products of ozone that form during the oxidation of compounds found in aqueous media are reviewed and more research is required before a valid assessment of the risks of ozone by-products can be made.
Abstract: The reaction products of ozone that form during the oxidation of compounds found in aqueous media are reviewed. Reaction products of ozone are well documented only for a limited number of substrates, and mechanistic information is quite rare. Decomposition of ozone during its reactions, sometimes induced by matrix impurities or by the by-products of the reactions, will generate highly reactive hydroxyl radicals. Thus, even reactions occurring at pH less than 7 may have radical character. More complete destruction of organic substrates may be enhanced by using catalysts, such as ultraviolet radiation or hydrogen peroxide, to accelerate radical formation. However, complete mineralization is generally not practical economically, so partially oxidized by-products can be expected under typical treatment conditions. Ozone by-products tend to be oxygenated compounds that are usually, but not always, more biodegradable and less toxic than xenobiotic precursors. Of particular interest are hydroperoxide by-products, which may have escaped detection because of their lability, and unsaturated aldehydes. Inorganic by-products tend to be in high oxidation states, which in some cases (e.g., some metallic elements) may lead to enhanced removal by flocculation and sedimentation. In other cases oxidation may lead to formation of reactive species such as hypobromous acid from bromide ion or permanganate from manganous ion. In general, more research is required before a valid assessment of the risks of ozone by-products can be made.
TL;DR: It is suggested that O-2, formed during phagocytosis, is converted to H2O2 within phagosomes and then diffuses out into the extracellular medium when its decomposition by catalase and/or peroxidases is blocked by azide.
TL;DR: In this paper, the development of a sensitive electrochemical assay for low levels of hydrogen peroxide is described, based on the enzymic reduction of substrate (H2O2) by peroxidase and subsequent electron transfer from a gold or pyrolytic graphite electrode to the enzyme via a redox mediator.
TL;DR: The results suggest that the degradation pathways of DNT in aqueous solution in the presence of hydrogen peroxide and UV light are side-chain oxidation, which converts DNT to 1,3-dinitrobenzene, and further photooxidation, which eventually converts the lower molecular weight acids and aldehydes to CO/sub 2/, H/ sub 2/O, and HNO/sub 3/.
Abstract: The synergistic effect of hydrogen peroxide and UV radiation from a medium-pressure mercury vapor lamp on the decomposition of 2,4-dinitrotoluene (DNT) in water was studied The results suggest that the degradation pathways of DNT in aqueous solution in the presence of hydrogen peroxide and UV light are (1) side-chain oxidation, which converts DNT to 1,3-dinitrobenzene, (2) hydroxylation of the benzene ring, which converts 1,3-dinitrobenzene to hydroxynitrobenzene derivatives, (3) benzene ring cleavage of these hydroxynitrobenzenes, which produces lower molecular weight carboxylic acids and aldehydes, and (4) further photooxidation, which eventually converts the lower molecular weight acids and aldehydes to CO/sub 2/, H/sub 2/O, and HNO/sub 3/
TL;DR: The toxicity of many redox-active compounds and their copper complexes appears to be due, at least partly, to the intracellular generation of hydrogen peroxide during oxidation of these compounds, an effect exacerbated by the ability of copper to inhibit catalase.
Journal Article•
TL;DR: Results obtained in the presence of glucose when glutathione was depleted with buthionine sulfoximine, diethyl maleate, or 1-chloro-2,4-dinitrobenzene were similar to results obtained when glutamate was depleted.
TL;DR: It is concluded that hydroxyl radicals are not likely the ultimate DNA strand-breaking species in cells exposed to extracellular superoxide anion and that the observed slow repair of DNA strand breaks may be significant in the mechanism of action of tumor-promoting agents.
Abstract: The repair kinetics and sensitivity to inhibitors of DNA strand breaks caused by superoxide anion, hydrogen peroxide, benzoyl peroxide and anthralin have been studied and compared with strand breaks caused by well-studied agents such as ionizing radiation and bleomycin. The latter two agents are generally believed to produce breaks indirectly by producing hydroxyl radicals, a very potent oxidizing species, which attack the phosphodiester backbone of DNA. As expected from earlier results, breaks induced by radiation and bleomycin rapidly disappear during post-treatment incubation as a consequence of the action of cellular DNA repair enzymes. Thus, strand breaks produced by hydroxyl radicals appear to be readily repaired in human leukocytes. By contrast, breaks caused by extracellular superoxide anion appeared not to be readily repaired, implying that some mechanism other than the generation of hydroxyl radicals in the vicinity of the DNA was involved. Inhibitors such as 3-aminobenzamide, cytosine arabinoside and adenine arabinoside affected the apparent rate of repair of radiation and methylmethane sulfonate-induced breaks but there was no indication that they affected superoxide anion-induced breaks. They partially inhibited repair of hydrogen peroxide-induced breaks. Breaks caused by benzoyl peroxide and anthralin were also apparently not repaired. We conclude that hydroxyl radicals are not likely the ultimate DNA strand-breaking species in cells exposed to extracellular superoxide anion and that the observed slow repair of DNA strand breaks may be significant in the mechanism of action of tumor-promoting agents.
TL;DR: The reaction kinetics of the peroxidase activity of prostaglandin H synthase have been examined with 15-hydroperoxyeicosatetraenoic acid and hydrogen peroxide as substrates and tetramethylphenylenediamine as cosubstrate.
TL;DR: A cup of coffee contains mutagens which produce about 5 X 10(4)-10(5) revertants of Salmonella typhimurium TA 100 without S9 mix, and one of them was identified to be methylglyoxal, which induced tumors in rats when administered by subcutaneous injection.
Abstract: A cup of coffee contains mutagens which produce about 5 X 10(4)-10(5) revertants of Salmonella typhimurium TA 100 without S9 mix. One of the mutagens was identified to be methylglyoxal. Methylglyoxal was present in various beverages such as black tea, whisky, and brandy. Methylglyoxal itself induced tumors in rats when administered by subcutaneous injection. However, the mutagenic properties of coffee were different from those of methylglyoxal. The mutagenicity of coffee was suppressed by catalase, and coffee was found to contain hydrogen peroxide. Furthermore, coffee solution was found to have a hydrogen peroxide-generating system. Instant coffee (15 mg/mL) contains 130 microM hydrogen peroxide immediately after the dissolution of coffee powder in water at room temperature. The concentration of hydrogen peroxide increased with time. The mutagenicity of methylglyoxal was increased by the copresence of hydrogen peroxide. A maximum of 30-fold enhancement was observed. The mutagenicity of black tea but not that of whisky was suppressed by catalase.
TL;DR: In this article, a new cytochemical technique based on a manganese dependent diaminobenzidine oxidation has been developed to detect superoxide in polymorphonuclear leukocytes, which is associated with the plasma membrane in cells activated by particulate (zymosan) and nonparticulate (phorbol myristate acetate) stimuli.
Abstract: Phagocytosis by polymorphonuclear leukocytes triggers a burst of oxidative metabolism resulting in hydrogen peroxide and superoxide production, and these active oxygen species function in the killing of microorganisms. A new cytochemical technique, based on a manganese dependent diaminobenzidine oxidation, has been developed to detect superoxide in these cells. It has been shown that superoxide generation is associated with the plasma membrane in cells activated by particulate (zymosan) and nonparticulate (phorbol myristate acetate) stimuli. This membraned activity is maintained during invagination such that reduced oxygen is generated within the endocytic vacuoles. Reaction product is absent from unstimulated cells; additionally, formation of precipitate is blocked by omission of Mn++, low temperature, glutaraldehyde prefixation, and the presence of superoxide dismutase in the incubation medium.