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PubMed1984

Myeloperoxidase reduces the opsonizing activity of immunoglobulin G and complement component C3b.

The effect of myeloperoxidase, hydrogen peroxide (H2O2) and a halide (Cl) on the opsonizing molecules in immunoglobulin G (IgG) and complement factor C3b was assayed. At concentrations of the enzyme (1 microgram/ml) that can be found in the extracellular fluid during inflammation, the myeloperoxidase-H2O2-Cl system inhibited the opsonizing effect of IgG and C3b measured as phagocytic uptake and superoxide generation. The effect was related to the enzymatic peroxidative activity of the protein. The presence of albumin (10 mg/ml) reduced the effect of myeloperoxidase with 10-20%. Taurine, which in the presence of myeloperoxidase-H2O2-Cl forms hydrophilic chloramines, and D-penicillamine, which scavenges HOCl, neutralize the inhibitory effect of myeloperoxidase. This suggests that either hypochlorous acid or lipophilic chloramines may exert its effect by oxidizing free sulphydryl groups exposed on the opsonizing ligands. Since the myeloperoxidase-H2O2-halide system also affects chemotactic factors, leukotrienes, proteinases and membrane receptors, the system may in several ways affect the development of the inflammatory response.

Complement C3b↗

PubMed1992

Lens opacification and H2O2 elevation induced by a tumor promoter.

Incubation of whole bovine lens with 10(-7) M 12-O-tetradecanoylphorbol-13-acetate (TPA) led to the lens opacity within 24 h. The hydrogen peroxide (H2O2) concentration in the whole lens was elevated 4 fold after treatment with either 10(-7) M TPA or 2.5 mM glucose/20 microM glucose oxidase. The lens opacification and H2O2 elevation were TPA dose-dependent. Preincubation of the lens with anti-tumor promoting agents EGCG (epigallocatechin gallate) or Sarp A (sarcophytol A) stopped the TPA-mediated opacification process and suppressed H2O2 elevation.

Animals↗

PubMedDate not supplied

Origin and development of hydrogen peroxide disinfection systems.

The discovery of hydrogen peroxide (H2O2) by Thénard in 1818, and the early phase of its development, are discussed. A brief description is given of the uses of this compound for purposes other than contact lens care. A detailed description of the first application of H2O2 to hydrophilic contact lenses is provided. A review of toxicologic and microbiologic issues and concerns follows, with specific emphasis on the decimal reduction rate (D-value) for H2O2 and the contribution of elements test as applied to any disinfection system. The role of pH and increasing concentrations of H2O2 in inducing ocular discomfort is described. After the introduction of the first H2O2 system, a number of competitive methods reached the marketplace. The unique qualities of one neutralization technique are noted. Hydrogen peroxide will continue for some time as a popular contact lens disinfection mechanism.

Animals↗

PubMed1990

Patterns of protein synthesis in a growth delay mutant (nuv) of Escherichia coli after treatment by near-UV radiation or hydrogen peroxide.

When Escherichia coli cells are stressed by hydrogen peroxide (H2O2), synthesis of a large number of proteins is repressed, while several other proteins are induced. Since there is evidence that some lethal effects of near-UV (NUV) radiation may be directly or indirectly due to hydrogen peroxide generated by NUV light, treatment of cells with NUV radiation or H2O2 might be expected to repress and induce the same set of proteins. In this study, we compared the effects of H2O2 and NUV irradiation on patterns of protein induction and/or repression which were separate from the 4-thiouridine-dependent response using growth delay mutants (nuv). Concentrating initially on the proteins that ceased synthesis following NUV irradiation in an nuv mutant, we observed that these were not the same as those that ceased synthesis following H2O2 treatment. Inspection of two-dimensional polyacrylamide gel electrophoresis proteins indicated that NUV irradiation repressed synthesis of a different set of proteins, although there was some overlap between the two (45%). It was also observed that the new proteins which appeared after each of the two treatments were different. This suggests that the induction and/or repression of new proteins following NUV irradiation is not triggered solely via oxidative stress, although there is some overlap between the proteins that are induced or repressed following the two treatments.

Bacterial Proteins↗

PubMed1989

Effect of hydrogen peroxide on guinea-pig tracheal smooth muscle in vitro: role of cyclo-oxygenase and airway epithelium.

1. Hydrogen peroxide (H2O2) (0.1 microM-3 mM) induced variable contractions of guinea-pig isolated trachea which were attenuated by catalase (100 u ml-1) and mannitol (15 mM) suggesting that contractions were induced by H2O2 and/or the hydroxyl anion. 2. Epithelial removal potentiated contractile responses of tracheal preparations to H2O2 with a leftward shift of the concentration-response curve and an increase in the maximal response. 3. Indomethacin (3 microM) inhibited contractions to H2O2 of intact preparations and preparations without epithelium suggesting that contractions may be mediated by cyclo-oxygenase products. Intact preparations (but not preparations without epithelium) contracted in response to high concentrations (greater than 0.1 mM) of H2O2 in the presence of indomethacin suggesting that other excitatory factor(s) released by the epithelium may induce contraction. 4. Preincubation of intact tracheal preparations with H2O2 (1 mM) for 1 h had no effect on responses to histamine or isoprenaline. 5. These results suggest that hydrogen peroxide generated during the inflammatory process may play a role in bronchoconstriction.

Animals↗

PubMed1985

Presence of lipid hydroperoxide in human plasma.

Using purified prostaglandin (PG) H synthase, which synthesizes PGG2 and PGH2 from arachidonic acid, we were able to assay for the presence of peroxide activators in biological tissues. This assay system, capable of detecting both hydrogen peroxide (H2O2) and lipid hydroperoxides, detected a significant amount of synthase activator in plasma. Treatment of the active preparations with catalase and glutathione peroxidase showed that the principal activator in normal human plasma was a lipid hydroperoxide rather than H2O2.

Catalase↗

PubMed1977

Effects of vitamin E on the platelet aggregation induced by combined adenosine diphosphate and hydrogen peroxide.

Hydrogen peroxide can either induce or inhibit or enhance the platelet aggregation in vitro depending upon the experimental conditions. Vitamin E and vitamin E-nicotinate are found to be effective to inhibit, to some extent, the platelet aggregation induced by combined adenosine diphosphate (ADP) and hydrogen peroxide (H2O2), added simultaneously, to the platelet rich plasma (PRP). Vitamin E and vitamin E-nicotinate seemed, however, to be unable to prevent the reduction of platelet response to ADP, which was brought about by the pretreatment of PRP with H2O2 of a lower concentration.

Adenosine Diphosphate↗

PubMed1990

Decreased in vivo survival of hydrogen peroxide-damaged baboon red blood cells.

In this study we attempt to establish the consequence of in vitro hydrogen peroxide (H2O2)-induced membrane damage as manifested by spectrin-hemoglobin (Sp-Hb) complex formation and decreased red blood cell (RBC) deformability to in vivo RBC survival in baboons. After exposure to 135 to 581 mumols/L H2O2 and reduction with dithiothreitol (DTE), baboon RBCs were infused into the animal, and the fraction of cells remaining in circulation after 24 hours and the lifespan of surviving cells were quantitated. In a dose-dependent fashion, a positive correlation was observed between in vitro membrane alterations and the 24-hour in vivo survival. While 12% of the control cells were removed from circulation in 24 hours, 23% were removed after treatment with 339 mumols/L H2O2, and 36% following exposure to 581 mumols/L H2O2. Pretreatment with carbon monoxide before exposure with H2O2 increased the survival of oxidized RBCs. RBCs not removed from circulation in the first 24 hours had a normal lifespan. Moreover, by selectively isolating biotin-labeled, peroxide-treated cells that survived the first 24-hour posttransfusion period, a significant decrease in Sp-Hb crosslinking was observed in these cells. These results suggest that a subpopulation of cells sensitive to oxidation were removed during the first 24 hours. To identify this population, the survival of density-fractionated RBCs exposed to oxidant stress was quantitated. No differences in either the 24-hour survival or RBC life span were observed between untreated low-density (MCHC less than or equal to 32g/dL) and high-density cells (MCHC greater than or equal to 37g/dL). However, striking differences were noted after treatment with 339 mumols/L H2O2, with the 24-hour survival of high-density cells showing a marked decrease compared with low-density cells. These data support our hypothesis that during peroxidative membrane damage, Hb oxidation initiates a sequence of events resulting in skeletal changes that lead to membrane alterations and, eventually, in vivo destruction, and that the dense, dehydrated cells are more susceptible to oxidant damage.

Animals↗

PubMed1992

Different modifications by vanillin in cytotoxicity and genetic changes induced by EMS and H2O2 in cultured Chinese hamster cells.

The modifying effects of vanillin on the cytotoxicity and 6-thioguanine (6TG)-resistant mutations induced by two different types of chemical mutagens, ethyl methanesulfonate (EMS) and hydrogen peroxide (H2O2), were examined using cultured Chinese hamster V79 cells. The effects of vanillin on H2O2-induced chromosome aberrations were also examined. Vanillin had a dose-dependent enhancing effect on EMS-induced cytotoxicity and 6TG-resistant mutations, when cells were simultaneously treated with vanillin. The post-treatment with vanillin during the mutation expression time of cells after treatment with EMS also showed an enhancement of the frequency of mutations induced by EMS. However, vanillin suppressed the cytotoxicity induced by H2O2 when cells were post-treated with vanillin after H2O2 treatment. Vanillin showed no change in the absence of activity of H2O2 to induce mutations. Post-treatment with vanillin also suppressed the chromosome aberrations induced by H2O2. The differential effects of vanillin were probably due to the quality of mutagen-induced DNA lesions and vanillin might influence at least two different kinds of cellular repair functions. The mechanisms by which vanillin enhances or suppresses chemical-induced cytotoxicity, mutations and chromosome aberrations are discussed.

Animals↗

PubMed1985

Metal ions and oxygen radical reactions in human inflammatory joint disease.

Activated phagocytic cells produce superoxide (O2-) and hydrogen peroxide (H2O2); their production is important in bacterial killing by neutrophils and has been implicated in tissue damage by activated phagocytes. H2O2 and O2- are poorly reactive in aqueous solution and their damaging actions may be related to formation of more reactive species from them. One such species is hydroxyl radical (OH.), formed from H2O2 in the presence of iron- or copper-ion catalysts. A major determinant of the cytotoxicity of O2- and H2O2 is thus the availability and location of metal-ion catalysts of OH. formation. Hydroxyl radical is an initiator of lipid peroxidation. Iron promoters of OH. production present in vivo include ferritin, and loosely bound iron complexes detectable by the 'bleomycin assay'. The chelating agent Desferal (desferrioxamine B methanesulphonate) prevents iron-dependent formation of OH. and protects against phagocyte-dependent tissue injury in several animal models of human disease. The use of Desferal for human treatment should be approached with caution, because preliminary results upon human rheumatoid patients have revealed side effects. It is proposed that OH. radical is a major damaging agent in the inflamed rheumatoid joint and that its formation is facilitated by the release of iron from transferrin, which can be achieved at the low pH present in the micro-environment created by adherent activated phagocytic cells. It is further proposed that one function of lactoferrin is to protect against iron-dependent radical reactions rather than to act as a catalyst of OH. production.

Arthritis, Rheumatoid↗

PubMed1989

Intestinal post-ischemic reperfusion injury: studies with neonatal necrotizing enterocolitis.

In the feline intestine studies have implicated superoxide (O.-) and other oxygen derived free radicals as initiators of injury as measured by increased capillary permeability during the reperfusion period. Biochemical mechanisms of this free radical generation include: xanthine oxidase dependent O.- production, hydrogen peroxide (H2O2) formation by superoxide dismutase (SOD), hydroxyl radical (OH-) production via the Haber-Weiss reaction, and lipid radical formation from membrane peroxidation. Pathological consequences of these events include inflammatory neutrophil infiltration, damage to the collagen and mucosal basement membrane, increased capillary permeability, edema, cell degeneration and necrosis. Animal models of neonatal necrotizing enterocolitis (NNEC) indicate that intestinal injury occurs after the etiologic factors (hypothermia, hypoxia) are removed. In order to determine the role of active oxygen species in the pathogenesis of NNEC, weanling hamsters and neonatal piglets were cold stressed and activities of pro/antioxidant enzymes were determined, and histopathologic and ultrastructural studies were performed. Cold stressed weanling hamsters showed a 55.7% (P less than 0.05) decrease in xanthine dehydrogenase/xanthine oxidase activity ratio. Light microscopy revealed scattered colonic mucosal erosions and submucosal edema in 50% of cold stressed animals. Transmission electron microscopy demonstrated degeneration of colonic mucosal epithelial cells, enlarged intracellular spaces, cytoplasmic vacuolization, and nuclear membrane swelling. The colonic serosa was also edematous and infiltrated with bacteria. Large intestinal tissue from cold stressed neonatal piglets showed a significant increase (P less than 0.05) in Mn and Cu, Zn, SOD, CAT, GSH-Red, total GSH, and Glc6-PD at 0 and 12 hrs. post stress.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1980

Evidence for participation of hydroxyl radical in increased microvascular permeability.

Polymorphonuclear leukocytes undergo the respiratory burst when exposed to a variety of stimuli. This is associated with the production of superoxide anion radical (O-2). Dismutation of O-2 can occur spontaneously to produce hydrogen peroxide (H2O2) and in the presence of metal catalysts O-2 and H2O2 can react to form hydroxyl radical (OH.). Some of these reactive species are released into the interstitium and may cause lipid peroxidation and depolymerization of macromolecules. We have studied the effect of free radicals on vascular permeability. Hypoxanthine and xanthine oxidase were applied topically on the hamster cheek pouch microcirculation model, injected intravenously with FITC-dextran 150 (Mw 150,000) to visualize permeability changes. This caused a flux of O-2 and a significant increase in macromolecular leakage. An attempt was made to elucidate the roles of different radicals by addition of superoxide dismutase (SOD), catalase (CAT), dimethyl sulfoxide (DMSO) and L-methionine to the reaction mixture. A significant decrease in leakage was found with all these substances, indicating OH. or possibly singlet oxygen damage. These results indicate that a free radical flux can cause permeability changes, and we suggest that part of the permeability change seen during inflammation may be related to free radical flux produced by activated leukocytes.

Animals↗

PubMedDate not supplied

Determination of absolute chemiluminescence quantum yields for reactions of bis-(pentachlorophenyl) oxalate, hydrogen peroxide and fluorescent compounds.

Absolute chemiluminescence quantum yields (phi CL) for reactions of bis-(pentachlorophenyl) oxalate (PCPO), hydrogen peroxide (H2O2) and 9:10 diphenyl anthracene (DPA) have been determined. A fully corrected chemiluminescence monitoring spectrometer was calibrated for spectral sensitivity using the chemiluminescence of the bis-(pentachlorophenyl) oxalate system as a liquid light source, the total photon output of which had previously been determined by chemical actinometry. At high (PCPO)/(H2O2) ratios phi CL was found to be independent of PCPO and H2O2 concentrations.

Anthracenes↗

PubMed1987

The biological activity of hydrogen peroxide. III. Induction of Epstein-Barr virus via indirect action, as compared with TPA and teleocidin.

Hydrogen peroxide (H2O2) was found to be a potent inducer of the production of the early antigen complex (EA) and/or virus capsid antigen (VCA), determined by Epstein-Barr virus (EBV). Maximum synthesis of EBV antigens was induced by 0.2 mM H2O2, 5 days after a single 10-min treatment, in both B95-8 cells (30.2%) and P3HR-I cells (17.4%). These induction frequencies by H2O2 of proteins encoded by the EBV genome were almost the same as those obtained by 10 min treatment with the potent inducers, 12-O-tetradecanoylphorbol-13-acetate (TPA) and teleocidin. In combination with n-butyrate (4mM), H2O2 showed an additive induction of EBV antigens (1.9- and 1.7-fold in B95-8 and P3HR-I cells, respectively) and was as efficient as TPA and teleocidin. H2O2 induced EBV antigens at a very low level (less than 1%) in Raji cells by itself, but it induced EBV antigens synergistically in combination with n-butyrate (about 25-fold). In combined treatments using H2O2, TPA and teleocidin, the combination of H2O2 and TPA or H2O2 and teleocidin showed additive effects on the induction of synthesis of EBV antigens, but the combination of TPA and teleocidin showed almost the same induction level as that produced by H2O2, TPA or teleocidin alone. The inducing activities of H2O2, TPA and teleocidin were suppressed completely, in the case of H2O2, and slightly, in the cases of TPA and teleocidin, by treatment with catalase. Moreover, the effects of H2O2 were largely suppressed by scavengers of hydroxyl radical (X OH) and singlet oxygen (1O2), but not by superoxide dismutase (SOD), whereas the induction of EBV proteins by TPA and teleocidin was largely suppressed by SOD, but only slightly by scavengers of X OH and 1O2. Thus, the biological actions of H2O2 on the activation of the EBV genome seem to be essentially different from those of TPA and teleocidin, though the biological actions of TPA and teleocidin may be partially ascribed to those of H2O2.

Animals↗

PubMed1992

Multicellular oxidant defense in unicellular organisms.

Although catalase is thought to be a major defense against hydrogen peroxide (H2O2), the catalase activity within individual Escherichia coli fails to protect against exogenous H2O2. Contrary to earlier reports, we find that dilute suspensions of wild-type and catalase-deficient E. coli are identical in their sensitivity to H2O2, perhaps because even wild-type, catalase-positive E. coli cannot maintain an internal/external concentration gradient of this highly diffusible oxidant. However, concentrated suspensions or colonies of catalase-positive E. coli do preferentially survive H2O2 challenge and can even cross-protect adjacent catalase-deficient organisms. Furthermore, high-density catalase-positive--but not catalase-negative--E. coli can survive and multiply in the presence of competitive, peroxide-generating streptococci. These observations support the concept that bacterial catalase may defend colonial, but not individual, E. coli against environmental H2O2. Group protection by the activity of enzymes that mitigate oxidative stress may have been a driving force in the evolution of multicellular organisms.

Biological Evolution↗

PubMed1984

Role of oxygen radicals in cardiac injury due to reoxygenation.

The ability of oxygen derived free radicals to induce irreversible cellular injuries during reoxygenation was studied on isolated potassium-arrested heart preparation. Enzymatic scavengers of hydrogen peroxide (H2O2) and superoxide anion (O-2), catalase and superoxide dismutase, were not effective in reversing the cardiac alterations induced by hypoxia. Cellular injuries induced by reoxygenation, 'Oxygen paradox', were partially prevented by scavengers of H2O2 (glutathione reduced form, catalase) and O-2 (superoxide dismutase). The 'oxygen paradox' was associated with a release of malonaldehyde. The inhibition of lipid peroxidation by alpha-tocopherol prevented the toxic effect of molecular oxygen on hypoxic hearts. The specific quenchers of singlet oxygen (histidine) and hydroxyl radical (mannitol) reduced the peroxidation of unsaturated lipids and the intensity of the 'oxygen paradox' phenomenon. The results indicate that in cardiac muscle (i) oxygen derived free radicals are important byproducts of abnormal oxidative metabolism present during the post hypoxic period; (ii) the 'oxygen paradox' phenomenon is related to the formation of lipid hydroperoxides leading to the cellular membrane disruption and to the irreversible alteration of cardiac integrity.

Adenosine Triphosphate↗

PubMed1977

Effect of hyperoxia on superoxide anion and hydrogen peroxide production of polymorphonuclear leucocytes and alveolar macrophages.

Hyperoxia activates superoxide dismutase (SOD) while inactivating catalase and glutathione peroxidase in polymorphonuclear leucocytes (PMN) and alveolar marcophages (AM) obtained from guinea-pigs exposed to 85% oxygen for 90 h. The influence of these altered enzyme activities on the rate of oxygen consumption and release of superoxide anion (O--2) and hydrogen peroxide (H2O2) was investigated. By 18 h O--2 released from resting PMN increased two-fold and remained elevated through the entire periods of the study, whereas H2O2 release and oxygen consumption at the same time points remained normal. At 66 h PMN phagocytizing opsonized zymosan particles released additional quantities of O--2 and H2O2 and consumed significantly more oxygen compared to the usual increase noted at earlier time points. Although oxygen consumption was almost two-fold higher in AM than PMN, phagocytizing AM released three-fold less O--2 and five-fold less H2O2 than did PMN. Furthermore, AM of animals exposed to hyperoxia no longer exhibited enhanced O--2 production upon exposure to opsonized zymosan. Hydrogen peroxide release progressively decreased at rest but progressively increased during phagocytosis of opsonized zymosan during the 90 h exposure to hyperoxia. No changes in oxygen consumption of AM occurred during hyperoxia. The divergent oxidative responses in PMN and AM of guinea-pigs exposed to hyperoxia suggest different biochemical adaptive mechanisms.

Animals↗

PubMed1991

Cross-adaptive response in Escherichia coli caused by pretreatment with H2O2 against formaldehyde and other aldehyde compounds.

A cross-adaptive response (CAR), defined as a reduction of the effects of an agent by pretreatment with another agent, was demonstrated when E. coli WP2 cells were pretreated with hydrogen peroxide (H2O2) followed by challenging treatment with aldehyde compounds. Pretreatment with a sublethal dose (60 microM) of H2O2 for 30 min made WP2 cells resistant to the killing effects of formaldehyde (FA), and 4 other mutagenic aldehydes: glutaraldehyde, glyoxal, methyl glyoxal and chloroacetaldehyde. CAR was also observed in WP2uvrA (uvrA-) and ZA12 (umuC-) cells, but not in ZA60 (recA-) and CM561 (lexA- (Ind-] cells. A role of recA and lexA in CAR was further suggested by the lack of beta-galactosidase induction in recA- and lexA- cells by H2O2. CAR and beta-galactosidase induction, however, were found to be separate events since CAR was recovered by introducing the recA+ gene into lexA- cells, but no induction of beta-galactosidase by H2O2 was observed in cells with the same gene transfer. These results suggest that H2O2 has the capacity to induce a function which reduces the killing effects of aldehydes, and the function is controlled by the recA gene without involvement of SOS response.

Acclimatization↗