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PubMed1986

The glutathione redox cycle as a defense system against hydrogen-peroxide-induced prostanoid formation and vasoconstriction in rabbit lungs.

Leukocyte-derived oxidants have been described as causing vasoconstriction and edema formation in isolated lungs. In the present study, dose-dependent and reversible pressor responses were achieved reproducibly by injection of hydrogen peroxide (H2O2) into the pulmonary artery of blood-free, perfused, isolated rabbit lungs in a dose-dependent manner. The pressor responses were accompanied by an instantaneous release of thromboxane A2 and a more delayed but quantitatively larger release of prostaglandin I2 into the recirculating perfusion fluid. There was no release of potassium or LDH, indicating the absence of overt cell damage. The H2O2-induced pressor responses were blocked by indomethacin (cyclooxygenase inhibitor), imidazole (inhibitor of thromboxane synthetase), mepacrine (phospholipase inhibitor), and W7 and trifluoperazine (agents that interfere with calcium-calmodulin function). Treatment with 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU) dose-dependently inhibited the lung glutathione reductase activity and augmented the metabolic (prostanoid release) and functional (vasoconstriction) responsiveness of the pulmonary vascular bed to H2O2. Application of 1-(2-chloroethyl)-1-nitrosourea (CCNU), a control to BCNU, and inhibition of catalase activity by aminotriazole did not increase the sensitivity to externally applied H2O2. We conclude that calcium-calmodium function and thromboxane generation may be involved in the pulmonary vasoconstrictive response to H2O2 and that the lung glutathione redox cycle is active in limiting the responsiveness of the pulmonary vascular bed to externally generated H2O2.

Animals↗
PubMed1992

On the mechanism of lipoxygenase-like action of bleomycin-iron complexes.

The mechanism of lipid peroxidation catalyzed by bleomycin (BLM)-iron (Fe) complexes has been studied in vitro using sodium linoleate as a substrate. BLM-Fe(II)-O2 and BLM-Fe(III) complexes catalyze lipid peroxidation concomitantly with singlet oxygen evolution. The results from spin trapping methods and gas chromatography-mass spectroscopy (GCMS) analyses suggest that the initial step of lipid peroxidation catalyzed by BLM-Fe complexes is similar to that of soybean lipoxygenase, viz., hydrogen abstration. However, another mechanism might be concerned in the case of BLM-Fe(II)-O2 complex. BLM-Fe complexes are also capable of enhancing singlet oxygen evolution from the hydrogen peroxide (H2O2)-hypochlorite (OCl-) system.

Bleomycin↗
PubMedDate not supplied

Data on oxidants and antioxidants.

The monovalent reduction of O2 gives rise to highly reactive O2 intermediates, such as superoxide radical (O2-.), hydrogen peroxide (H2O2), and hydroxyl radical (OH.), as well as to singlet O2 (1O2). These O2 metabolites are capable of acting on several groups of substances: enzymes to inactivate them, polyunsaturated fatty acids to form lipid peroxides and DNA to cause single strand breaks and mutations. There are, however, several lines of antioxidant defences, which can be enzymatic (superoxide dismutase, catalase, glutathione peroxidase) or non-enzymatic (glutathione, vitamins C and E, beta-carotene, etc.). These defences are necessary to protect the cell against the intracellular or extracellular generation of O2 metabolites. Since O2 intermediates can affect the general cellular metabolism and inhibit cell replication or reduce protein synthesis, all the biological effects of O2 and its metabolites should therefore be considered in the pathogenesis of emphysematous lesions in the lung.

Free Radicals↗
PubMed1991

Prevention of H2O2 generation by monoamine oxidase protects against CNS O2 toxicity.

Toxicity to the central nervous system (CNS) by hyperbaric oxygen (HBO) presumably relates to increased production of reactive oxygen species. The sites of generation of reactive oxygen species during HBO, however, have not been fully characterized in the brain. We investigated the relationship between regional generation of hydrogen peroxide (H2O2) in the brain in the presence of an irreversible inhibitor of catalase, aminotriazole (ATZ), and protection from CNS O2 toxicity by a monoamine oxidase (MAO) inhibitor, pargyline. At 6 ATA of oxygen, pargyline significantly protected rats from CNS O2 toxicity whereas ATZ enhanced O2 toxicity. In animals pretreated with ATZ, HBO inactivated 21-40% more catalase than air exposure in the six brain regions studied. Because ATZ-mediated inactivation of catalase was H2O2 dependent, the decrease in catalase activity during hyperoxia was proportional to the intracellular production of H2O2. Pargyline, administered 30 min before HBO, inhibited MAO by greater than 90%, prevented ATZ inhibition of catalase activity during HBO, and reversed the augmentation of CNS O2 toxicity by ATZ. These findings indicate that H2O2 generated by MAO during hyperoxia is important to the pathogenesis of CNS O2 toxicity in rats.

Amitrole↗
PubMed1990

Hydrogen peroxide localization in experimental optic neuritis.

The association of reactive oxygen species to altered permeability of the blood-brain barrier in acute experimental encephalomyelitis was investigated by ultrastructural cytochemical localization of hydrogen peroxide (H2O2) to sites in the optic nerve previously identified by extravasation of intravascular horseradish peroxidase. Using a modified cerium method, we found electron-dense cerium-derived H2O2 reaction product was localized to the perivascular space at the lamina retinalis, lamina choroidalis, and lamina scleralis. In the optic nerve head, electron-dense reaction product was observed in the presence of intravascular leukocytes, although adjacent perivascular and interstitial inflammatory cells at this site were scant. In the myelinated retrobulbar optic nerve, cerium-derived H2O2 reaction product was seen in the intravascular space of blood vessels and surrounding perivascular and interstitial foci of inflammatory cells. Reaction product was also observed in the extracellular space adjacent to the plasmalemma of axons and glial cells in the optic nerve head and retrobulbar nerve. The perivascular and intravascular distribution of cerium-derived reaction product suggests that H2O2 may play a role in the pathogenesis of altered vascular permeability in experimental optic neuritis and supports our previous observations of suppression of blood-brain barrier permeability by detoxification of H2O2 with the exogenous administration of antioxidant enzymes.

Animals↗
PubMed1986

Copper ions and hydrogen peroxide form hypochlorite from NaCl thereby mimicking myeloperoxidase.

Sea urchins have elaborated multiple defenses to assure monospermic fertilization. In this work, we have concentrated on a study of the mechanism(s) by which hydrogen peroxide (H2O2) prevents polyspermy in Arbacia punctulata. We found that it is not H2O2 but probably hypochlorous acid/hypochlorite (HOCl/OCl-) derived from H2O2 that is toxic to the supernumerary sperm. The spermicidal activity of H2O2 is potentiated by at least one order of magnitude by cupric ions (Cu2+). This increased toxicity is not due to the formation of hydroxyl radicals (.OH) because .OH scavengers did not counteract the activity of Cu2+. Moreover, substitution of Cu2+ by ferrous ions (Fe2+), which are known to cause formation of .OH from H2O2, had no effect on fertilization even at 10(2)-10(3) times higher concentrations. In contrast, 3-amino-1,2,4-triazole (AT), and HOCl/OCl- scavenger, totally reversed the toxic effects of Cu2+. Furthermore, we found that HOCl/OCl- is generated in solutions of H2O2 and Cu2+ in the presence of 0.5 M NaCl and that its accumulation is abolished by AT. Thus it is possible that the antifertility properties of copper are due to its ability to mediate formation of HOCl/OCl-. HOCl/OCl- generated by Cu2+ from H2O2 and Cl-, a low concentration of exogenously added HOCl/OCl-, or increased concentrations of H2O2 has similar inhibitory effects on the fertilization process in sea urchins. Therefore, we suggest that polyspermy is prevented by the action of a myeloperoxidase that affects the formation of HOCl/OCl- from the Cl- present in sea water through reaction with H2O2 generated by the newly fertilized egg.

Amitrole↗
PubMed1985

Participation of active oxygen species in the induction of chromosomal aberrations by cadmium chloride in cultured Chinese hamster cells.

The effect of various scavengers of active oxygen species on the induction of chromosomal aberrations by cadmium chloride (CdCl2) was investigated in cultured Chinese hamster V79 cells. Incidences of chromosomal aberrations by CdCl2 were partially or fully reduced by the presence of catalase, mannitol (a scavenger of hydroxyl radicals) and butylated hydroxytoluene (BHT, an antioxidant). These findings may indicate participation of the active oxygen species such as hydrogen peroxide (H2O2) or hydroxyl radicals in the clastogenicity of cadmium. In contrast, superoxide dismutase (SOD) and dimethylfuran (a scavenger of singlet oxygen) did not influence incidences of chromosomal aberrations by CdCl2. These results suggest that superoxide anion and singlet oxygen are not directly involved in the clastogenicity of the metal. The presence of aminotriazole (an inhibitor of catalase) increased incidences of chromosomal aberrations by CdCl2. This emphasizes participation of H2O2 in the clastogenicity of cadmium.

Animals↗
PubMed1986

Changes in synaptic transmission produced by hydrogen peroxide.

The effect of hydrogen peroxide (H2O2) on excitatory and inhibitory synaptic transmission was studied at the lobster neuromuscular junction. H2O2 produced a dose dependent decrease in the amplitude of the junction potential (Vejp). This decrease was due to changes in both presynaptic transmitter release and the postsynaptic response to the neurotransmitter. Observed presynaptic changes due to exposure to H2O2 were a decrease in the amount of transmitter released, that is, quantal content, as well as a decrease in the fast facilitation, that is, the amplitude increase of successive excitatory junction potentials at a rate of 3 Hz. To discern postsynaptic changes, glutamate, the putative excitatory neurotransmitter for this preparation was applied directly to the bathing medium in order to bypass the presynaptic release process. H2O2 produced a decreased response of the glutamate receptor/ionophore. The action of H2O2 was not selective to excitatory (glutamate-mediated) transmission because inhibitory (GABA-mediated) transmission was also depressed by H2O2. This effect was primarily presynaptic since H2O2 produced no change in the postsynaptic response to applied GABA.

Animals↗
PubMed1991

Synergistic induction of ovulation and prostaglandin synthesis in goldfish (Carassius auratus) follicles by sodium orthovanadate and hydrogen peroxide.

The effects of hydrogen peroxide (H2O2) and sodium orthovanadate (Na3VO4) on ovulation and prostaglandin (PG) production were investigated in goldfish (Carassius auratus) follicles. H2O2, at levels that did not stimulate ovulation, significantly increased the ability of Na3VO4 to induce ovulation. The enhancing effect of H2O2 on Na3VO4-induced (10 microM) ovulation was observed over a wide range of concentrations (0.3-19.2 ppm) but was maximal at 1.2-4.8 ppm. The H2O2 effect on ovulation diminished at concentrations greater than 4.8 ppm. Na3VO4 and H2O2 also stimulated prostaglandin E (PGE) and prostaglandin F (PGF) levels in incubates. An interactive effect of the two agents was significant only on PGE production. However, optimal H2O2/Na3VO4 concentrations for the stimulation of PG production were much higher than those for stimulating ovulation. In most incubations, Na3VO4-induced or Na3VO4/H2O2-induced ovulation was not inhibited by the cyclooxygenase inhibitor indomethacin (IM), but was blocked by the lipoxygenase inhibitor nordihydroguaiaretic acid (NDGA). Treatment of an Na3VO4/H2O2 mixture with catalase before the start of incubation totally abolished the enhancing effect of H2O2 on ovulation. This suggests that the enhancing effect of H2O2 on ovulation may not be a result of a chemical metabolite(s) produced by the two agents in mixture but rather is due to some direct effect of H2O2. This may have physiological significance in light of the published effects of H2O2 on various processes known to be involved in ovulation.

Animals↗
PubMed1984

Direct measurement of hydrogen peroxide release from rat alveolar macrophages: artifactual effect of horseradish peroxidase.

Investigators disagree on the amount of hydrogen peroxide (H2O2) released by resting and stimulated alveolar macrophages. The method commonly used to measure H2O2 release involves horseradish peroxidase (HRP)-catalyzed oxidation of scopoletin by H2O2. We describe an artifact in this method that may explain the seemingly inconsistent data reported by other investigators. Release of H2O2 and luminol-catalyzed chemiluminescence are stimulated in rat alveolar macrophages by type II HRP at concentrations normally used in the HRP-scopoletin method. The amount of H2O2 released depends upon the length of time the cells are preincubated at 37.5 degrees C and the time at which type II HRP is added. After stimulation with type II HRP, the cells do not release additional H2O2 upon exposure to zymosan particles. Myeloperoxidase, an alternative catalyst to type II HRP, does not stimulate H2O2 release and, therefore, can be used to measure H2O2 release from rat alveolar macrophages. Using myeloperoxidase, resting H2O2 release is negligible; after zymosan stimulation, 6.14 (+/- 0.87) X 10(-6) nmoles/cell X 10 min is released. In addition, more pure HRP preparations (types VI, VII, VIII, and IX) do not stimulate alveolar macrophages to release H2O2 and can be used to monitor zymosan-induced H2O2 release. As our data indicate that type II HRP stimulates H2O2 release from rat and guinea pig alveolar macrophages, it is not the catalyst of choice for this assay. In conclusion, our data explain the conflicting results found in the literature and indicate that rat alveolar macrophages release minimal amounts of H2O2 at rest and can be stimulated by zymosan.

Animals↗
PubMed1992

Glomerular injury induced by hydrogen peroxide: modifying influence of ACE inhibitors.

The sensitivity of isolated glomeruli from normotensive (Wistar-Kyoto, WKY) and spontaneously hypertensive (SHR) strains to oxidant stress was studied by determining the incidence of pyknosis, karyohexis and karyolysis after incubation with different concentrations of hydrogen peroxide (H2O2) (4.7 x 10(-9) - 10(-3) M). Even though the proportion of glomeruli containing nuclei that demonstrated these features increased progressively with increasing concentrations of H2O2, the number of severely damaged glomeruli was relatively small even at concentrations of 4.7 x 10(-3) M. Examination of the surface epithelial cells of glomeruli using scanning electron microscopy revealed no evidence of disturbance of the macroscopic or podocyte structure or, of increased blebbing after H2O2-treatment. These data suggest damage to nuclei is an early result of ROS stress on glomeruli. Preincubation of WKY glomeruli with captopril or lisinopril resulted in a significant drop in the proportion of WKY glomeruli demonstrating structural damage after oxidant stress. In contrast, preincubation of SHR glomeruli with lisinopril had no effect on oxidant-induced changes in the morphology of SHR glomeruli, whereas captopril effected a significant increase in the proportion of glomeruli demonstrating damage at all concentration of H2O2.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1989

Glomerular macrophages produce reactive oxygen species in experimental glomerulonephritis.

The production of reactive oxygen species by intraglomerular macrophages was assessed in a macrophage dependent model of diffuse proliferative glomerulonephritis in rabbits. Glomerular macrophages were obtained from isolated nephritic glomeruli by short term (60 min) culture. Control macrophage populations were simultaneously obtained from peripheral blood (blood monocytes) and lung lavage fluid (alveolar macrophages). Superoxide anion (O2-), hydrogen peroxide (H2O2) and hydroxyl radical (OH.) production was assessed. Glomerular macrophage production of O2- (48.9 +/- 5.5 nmol/hr/10(6) cells), H2O2 (4.4 +/- 2.5 nmol/hr/10(6) cells) and OH. (57.8 +/- 4.7 U/hr/10(6) cells) was significantly greater than the production of reactive oxygen species seen with control monocyte populations: alveolar macrophages, O2- 9.8 +/- 2.0 nmol/hr/10(6) cells; H2O2 0.6 +/- 0.3 nmol/hr/10(6) cells; OH. 11.0 +/- 1.8 U/hr/10(6) cells; blood monocytes, O2- 8.6 +/- 1.4 nmol/hr/10(6) cells; OH. 9.9 +/- 1.2 U/hr/10(6) cells, (all P less than 0.05 cf. glom macs). Hydrogen peroxide production by blood monocytes (1.6 +/- 0.9 nmol/hr/10(6) cells) was less than glomerular macrophages, however this difference was not statistically significant. The enhanced production of reactive oxygen species by glomerular macrophages in this macrophage dependent model of glomerulonephritis suggests that these mononuclear cells are locally activated within the glomerulus following recruitment from the circulation. Reactive oxygen species production by glomerular macrophages may contribute to their ability to induce glomerular basement membrane injury in this disease.

Animals↗
PubMed1979

Defective hydrogen peroxide production in chronic granulocytic leukaemia neutrophils.

Hydrogen peroxide (H2O2) production by polymorphonuclear neutrophils (PMN) during phagocytosis was fluorometrically vestimated over an incubation period of 80 min during which dead Candida guilliermondii were ingested. Ten patients with chronic granulocytic leukaemia (CGL) were tested and compared with 15 normal subjects. The production of H2O2 by CGL neutrophils was about 29% of normal. There was no correlation between H2O2 production and the impaired killing of Candida guilliermondii by the neutrophils of CGL patients.

Candida↗
PubMed1989

Induction of stress proteins in cultured human RPE-derived cells.

The expression and induction of stress protein families were examined in cultured human fetal retinal pigment epithelial (RPE)-derived cells. These stress proteins (SPs) include the heat-shock proteins (HSPs) that have been shown to be highly inducible following treatment by heat, amino acid analogues, and various chemical oxidants. Three sets of proteins with molecular weights of 70, 84, and 110 kilodaltons were elevated simultaneously from constitutive levels after treatment with azetidine-2-carboxylic acid (AzC), an amino acid analogue of proline. Further experiments demonstrated that incubation of cultured human fetal RPE-derived cells with hydrogen peroxide (H2O2) at concentrations ranging from 10(-5) M to 10(-3) M for 30 minutes to 60 minutes did not elevate the levels of the common families of HSPs as with AzC. These results indicate that cultured human fetal RPE-derived cells are capable of elevated HSP biosynthesis after AzC exposure but appear resistant to H2O2 treatment.

Azetidinecarboxylic Acid↗
PubMed1982

The involvement of hydroxyl radical derived from hydrogen peroxide in lignin degradation by the white rot fungus Phanerochaete chrysosporium.

The possible involvement of hydrogen peroxide (H2O2)-derived hydroxyl radical (.OH) in lignin degradation ([14C]lignin leads to 14CO2) by Phanerochaete chrysosporium was investigated. When P. chrysosporium was grown in low nitrogen medium (2.4 mM N), an increase in the specific activity for H2O2 production in cell extracts was observed to coincide with the appearance of ligninolytic activity and both activities appeared after the culture entered stationary phase. The production of .OH in ligninolytic cultures of P. chrysosporium was demonstrated by alpha-keto-gamma-methiolbutyric acid-dependent formation of ethylene. Hydrogen peroxide-dependent .OH formation was also shown in cell extracts of ligninolytic cultures. The radical species was demonstrated to be .OH by the .OH-dependent hydroxylation of p-hydroxybenzoic acid to form protocatechuic acid and by using 5,5-dimethyl-1-pyrroline-N-oxide and detecting the production of the nitroxide radical of 5,5-dimethyl-1-pyrroline-N-oxide by EPR. These reactions were inhibited by .OH-scavenging agents and were stimulated when azide was added to inhibit endogenous catalase. Lignin degradation by P. chrysosporium was markedly suppressed in the presence of the .OH-scavenging agents mannitol, benzoate, and the nonspecific radical scavenging agent butylated hydroxytoluene. The above results indicate that .OH derived from H2O2 is involved in lignin biodegradation by P. chrysosporium.

Agaricales↗
PubMed1993

Differential effects of reactive oxygen species on native synovial fluid and purified human umbilical cord hyaluronate.

The ability of reactive oxygen species produced by triggered neutrophilic leukocytes, hypoxanthine/xanthine oxidase (HX/XAO), hydrogen peroxide, and hypochlorous acid/myeloperoxidase (HOCl/MPO) systems to degrade hyaluronate (HA) in human synovial fluid (SF) and purified umbilical cord HA was compared by measuring the molecular weight distribution of HA using high-performance liquid chromatography with a size-exclusion column. The exposure of noninflammatory SF to phorbol myristic acetate (PMA)-activated neutrophils or to hydrogen peroxide (H2O2) caused depolymerization of SF HA to the degree corresponding to that found in rheumatoid SFs. When HX/XAO was used as radical generator, the molecular weight of SF HA decreased from 3.42 x 10(6) to 1.40 x 10(4) daltons with concomitant decrease of SF viscosity to 36% from the original value. The HOCl/MPO system caused no depolymerization of SF HA, even at very high unphysiological HOCl concentrations that induced the precipitation of SF HA together with SF proteins. This effect was found to be comparable to conventional mucin clot formation in SF. However, purified human umbilical cord HA was easily depolymerized with HOCl/MPO or with H2O2, but these effects were sensitive to the hydroxyl radical scavenger mannitol and iron chelator desferrioxamine, indicating that the formation of reactive hydroxyl radical (OH.) is likely to participate in these reactions. Thus we conclude that in inflammatory SF HA is mainly depolymerized by OH. produced by decomposition of H2O2 catalyzed by iron, free or locally bound to HA itself. In contrast to what has been reported earlier, HOCl/MPO only depolymerizes purified umbilical cord HA (in a hydroxyl radical-dependent manner) but does not depolymerize HA in SF. As a matter of fact, HOCl/MPO has a scavenging action on SF HA by consuming H2O2 and thus preventing the formation of reactive hydroxyl radicals.

Chemical Precipitation↗
PubMed1991

Hydrogen peroxide reduces beta-adrenoceptor function in the rat small intestine.

Incubation of isolated rat intestinal segments with hydrogen peroxide (H2O2) led to a decreased beta-adrenoceptor response. The maximal relaxation induced by isoprenaline was lowered while the EC50 remained unaffected. The effect of H2O2 in the small intestine increased slightly from duodenum to ileum. In the ileum, 10(-4) M H2O2 led to a 10% decrease of the maximal relaxation due to isoprenaline and 1 mM decreased the maximal response to about 50%. We further investigated the level at which the isoprenaline response was impaired. The relaxation caused by the stable cAMP analog, dibutyryl-cAMP, or by the adenylate cyclase activator, forskolin, was not affected or affected less than by isoprenaline. When the response to isoprenaline was expressed relative to the maximal response to dibutyryl-cAMP or forskolin, pretreatment with H2O2 led to a decreased isoprenaline response relative to the response to dibutyryl-cAMP or forskolin. This might indicate that exposure to H2O2 leads to a disturbance in receptor-mediated cAMP production. The adenylate cyclase unit is probably not affected since the response to forskolin is relatively resistant to H2O2. Our conclusion is that pretreatment of isolated intestinal segments with H2O2 leads to disturbed beta-adrenoceptor coupling, probably due to altered membrane integrity.

Animals↗
PubMed1995

Hydrogen peroxide preferentially enhances the tyrosine phosphorylation of epidermal growth factor receptor.

We found that hydrogen peroxide (H2O2) enhances EGF receptor tyrosine phosphorylation in intact cells as well as solubilized membrane of an EGF receptor hyperproducing cell line NA. An antioxidant MnCl2 effectively inhibited this enhancement. Interestingly, overall phosphorylation of the EGF receptor enhanced by H2O2 was half that of the EGF-enhanced phosphorylation when the receptor immunoprecipitated from [32P]orthophosphate-labeled cells was examined. Tryptic phospho-peptide mapping of these receptors revealed that EGF enhanced the phosphorylation on five specific residues including serine 671, 1,046 and 1,047, threonine 669 and tyrosine 1,173, whereas H2O2 enhanced the phosphorylation remarkably on tyrosine 1,173 and three other residues and only moderately on serine 1,046 and 1,047 and threonine 669. Thus, H2O2 preferentially enhances the tyrosine phosphorylation of EGF receptor through oxidant stress.

Amino Acid Sequence↗