Showing papers on "Hydrogen peroxide published in 1986"

Endothelial cell injury due to copper-catalyzed hydrogen peroxide generation from homocysteine.

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.

Selective oxidation of aldehydes to carboxylic acids with sodium chlorite-hydrogen peroxide

Abstract: Oxydation de cinnamaldehydes, benzaldehydes, furfural, pyridinecarbaldehyde-4, thiophenecarbaldehyde-2, pyrrolecarbaldehyde-2, alcenals, dans l'acetonitrile et dans differents solvants alcooliques

Hydrogen peroxide-inducible proteins in Salmonella typhimurium overlap with heat shock and other stress proteins.

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.

Preparation and Characterization of Chloramines

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.

A chemical mechanism for use in long‐range transport/acid deposition computer 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.

Role of hydrogen peroxide and hydroxyl radical formation in the killing of Ehrlich tumor cells by 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.

Hydrogen peroxide plasma sterilization system

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.

Microassays for superoxide and hydrogen peroxide production and nitroblue tetrazolium reduction using an enzyme immunoassay microplate reader.

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.

Henry's law determinations for aqueous solutions of hydrogen peroxide, methylhydroperoxide, and peroxyacetic acid

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.

Reaction Products of Ozone: A Review

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.

Photooxidation of 2,4-dinitrotoluene in aqueous solution in the presence of hydrogen peroxide.

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/

DNA strand breaks in human leukocytes induced by superoxide anion, hydrogen peroxide and tumor promoters are repaired slowly compared to breaks induced by ionizing radiation.

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.

Mutagens in coffee and other beverages.

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.

Superoxide production by polymorphonuclear leukocytes. A cytochemical approach.

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.

Myeloperoxidase as an effective inhibitor of hydroxyl radical production. Implications for the oxidative reactions of neutrophils.

Abstract: Hydroxyl radicals have been generated from hydrogen peroxide and superoxide (produced with xanthine oxidase), and an iron (EDTA) catalyst, and detected with deoxyribose, or in some cases with benzoate or alpha-keto-gamma-methiolbutyric acid. Purified myeloperoxidase, and neutrophils stimulated with fMet-Leu-Phe and cytochalasin B, strongly inhibited this hydroxyl radical production in a concentration-dependent manner. Supernatants from stimulated cells also inhibited, and inhibition by cells or supernatant was prevented by azide. There was much less inhibition by myeloperoxidase-deficient neutrophils. Inhibition thus was due to myeloperoxidase released by the cells. With neutrophils stimulated with phorbol myristate acetate, which release very little myeloperoxidase, hydroxyl radical production was enhanced due to the additional superoxide produced by the cells. It is concluded that under conditions where neutrophils release myeloperoxidase as well as superoxide and hydrogen peroxide, breakdown of hydrogen peroxide by myeloperoxidase would make conditions unfavorable for hydroxyl radical production.

Mechanisms of the reactions of some copper complexes in the presence of DNA with superoxide, hydrogen peroxide, and molecular oxygen.

Abstract: The kinetics and the reaction mechanism of some copper complexes of l,IO-phenanthroline, 5-nitrc1, IO-phenanthroline, and 2,2’-bipyridine with 02-, Hz02, and O2 in the presence of calf thymus DNA have been investigated with use of the pulse radiolysis technique. We have found that both copper(I1) and copper(1) complexes bind to DNA. The ternary complexes react very slowly with 02relative to the free complexes, while the rates of the oxidation of free and bound cuprous complexes by H202 are almost the same. Therefore these ternary copper complexes turned out to be good catalysts of the reaction between 02and Hz02. A complex between the chelating agent 1,lO-phenanthroline (OP) and copper(I1) is able to induce the degradation of DNA in the presence of a reducing agent.’-’ N o primary sequence specificity is apparent in the scission reaction* which proceeds under a variety of experimental conditions. These include incubtation of DNA, OP, and copper(I1) ions with the following: (a) reducing agents such as thiol or ascorbate in the presence of molecular oxygen;’” (b) systems generating the superoxide radical in the presence of molecular o ~ y g e n ; ~ . ~ (c) NADH and hydrogen pero~ide;~.’ (d) reducing agents and hydrogen p e r o ~ i d e . ~ The degradation of DNA was inhibited by intercalating agents and any reagent which reduced the concentration of either the cuprous complex (e.g., neocupr~ine)*-~g~ or hydrogen peroxide (e.g., ~a ta lase) .~” The sensitivity of the reaction to other inhibitors depended on the pathway for the generation of the cuprous complex and hydrogen peroxide (e.g., superoxide dismutase (SOD) inhibited the reaction potentiated by NADH and hydrogen peroxide but had no effect where thiol and hydrogen peroxide were p r e ~ e n t . ~ ~ 5-NO2-OP and 5-CLOP were more effective than OP in cleaving DNA while 5-CH3-OP was less effective than OP under comparable conditions.’,’ The cuprous complex of 2,2’-bipyridine (bpy) was unable to degrade DNA at similar concentrations used for OP,3-5 although the coordination chemistry, the kinetics, and the mechanism of the oxidation of this complex by oxygen and hydrogen peroxide are similar to that of OP.93’0 Moreover, it is known that complexes of bpy as well as those of OP bind to The reaction mechanism for this process has not yet been determined. It is believed that the cuprous complex intercalates with DNA and that the subsequent oxidation by hydrogen peroxide causes the damage due to the formation of OH. at the binding site.4” The binding constants of the various copper complexes to DNA and the kinetics and mechanism of the oxidation of the ternary complexes by oxygen, hydrogen peroxide, and superoxide radicals have not yet been determined. The understanding of the kinetics and mechanism of these reactions may shed light on the mechDNA.” ( I ) DAurora, V.; Stern, A. M.; Sigman, D. S. BBRC 1977, 78, 170. (2) Sigman, D. S.; Graham, D. R.; DAurora, V.; Stern, A. M. J . Biol. (3) Doweny, K. M.; Que, B. G.; So, A. G. BBRC 1980, 93, 264. (4) Que, B. G.; Doweny, K. M.; So, A. G. Biochemistry 1980, 19, 5987. (5) Marshall, L. E.; Graham, D. R.; Reich, K. A.; Sigman, D. S . Bio(6) Gutteridge, J. M.; Halliwell, B. Biochem. Phormacol. 1982. 31, 2801. (7) Reich, K. A,; Marshall, L. E.; Graham, D. R.; Sigman, D. S. J . Am. (8) Pope, L. M.; Reich, K. A,; Graham, D. R.; Sigman, D. S . J . Biol. (9) Goldstein, S.; Czapski, G. J . Am. Chem. Sot . 1983, 105, 7276. (IO) Goldstein, S . ; Czapski, G. Inorg. Chem. 1985, 24, 1087. ( 1 I ) Howe-Grant, M.; Lippard, S . J. Biochemisfry 1979, 18, 5762. Chem. 1979, 254, 12269. chemistry 1981, 20, 244. Chem. SOC. 1981, 103, 3582. Chem. 1982, 257, 12121. anism of DNA cleavage initiated by the various copper complexes. Experimental Section Materials. All chemicals employed were of analytical grade and were used as received: calf thymus DNA, type I, 2,2’-bipyridine, and sodium formate (Sigma Chemical Co.), l,lO-phenanthroline, 5-nitrophenanthroline (Fluka), H202 (Merck), SOD (Diagnostic Data Int.), cupric sulfate, monosodium and disodium phosphate (Mallinckrodt). All solutions were prepared in distilled water which was further purified by a Millipore reagent grade water system. A stock solution of DNA was prepared as 1 mg/mL containing 1 mM sodium phosphate buffer at pH 7. The concentration of DNA per nucleic acid phosphate was determined spectrophotometrically at 260 nm with z = 6875 M-’ cm-‘.I2 The cuprous complexes were generated by using the pulse radiolysis technique in oxygenated solutions containing 0.02 M sodium formate and 1 mM sodium phosphate buffer at pH 7. Under these conditions all the radicals formed by irradiation reduce the cupric c~mplexes . ’~’~ Kinetic studies were followed at 435 nm, where the various cuprous complexes a b s ~ r b . ~ . ’ ~ The concentration of H202 was determined with ferrous ~ u l f a t e . ’ ~ Apparatm. UV-visible absorption spectra were recorded with a Bauch and Lomb Model Spectronic 2000 spectrophotometer. The pulse radiolysis setup consisted of a Varian 7715 linear accelerator. The pulse duration ranged from 0.1 to 1.5 p s with a 200 mA current of 5 MeV electrons. The total concentration of the various cuprous complexes produced per pulse (1-15 pM) was evaluated with the use of a (0P),Cu2+ dosimeter. The yield of (OP)2Cu+ in oxygenated formate solution was assumed to be G = 6.05 and c = 6770 M-’ cm-’ at 435 Irradiation was carried out in a 2 cm long optical spectrosil cell with use of three light passes. A 150-W xenon lamp was used as the analytical light source and appropriate light filters were used to avoid photochemistry and to eliminate any scattered light. The detection system included a grating monochromator and an IP28 photomultiplier. The signal was transferred to a Nova 1200 minicomputer via either a Biomation 8100 or an analog-to-digital converter. The analysis of the data was carried out with the Nova 1200 minicomputer. Results and Discussion A. ”be Reduction of Copper(I1) by 0, in the Presence of DNA. In the irradiation of aqueous solutions containing formate ions and oxygen, the superoxide radical is p r ~ d u c e d . ’ ~ . ’ ~ As the pK of H02 is 4.8,I4J6 the reducing radical is mainly 02at pH 7. When the cupric complexes of OP, 5-N02-OP, or bpy (CuL?’) are present in excess relative to [02-],, reaction 1 takes place: ki CUL22+ + 0 2 CUL2+ + 0 2 (1) (12) Felsenfeld, G.; Hirschman, S. Z . J . Mol. Biol. 1965, 13, 407. (13) Matheson, M. S.; Dorfman, L. M. “Pulse Radiolysis”; MIT Press: (14) Bielski, B. H. J. Photochem. Photobiol. 1978, 28, 645. (15) Holm, N. W.; Berry, R. J. “Manual on Radiation Chemistry“; Marcel (16) Behar, D.; Czapski, G.; Rabani, J . ; Dorfman, L. M.; Schwartz, H. Cambridge, MA, 1969. Dekker Inc.: New York, 1970; pp 313-317. A. J. Phys. Chem. 1970, 74, 3209. 0002-7863/86/ 1508-2244$01.50/0