Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P04040 (Catalase)
3,577 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Neutrophils activated by soluble particulate stimuli generate superoxide anion and subsequently form hydrogen peroxide and other oxygen radicals. The effect of hydrogen peroxide on the complement system in normal serum was investigated. Treatment of normal serum with hydrogen peroxide resulted in a diminution of the haemolytic activity of the total and alternative complement pathways and the haemolytic titres of C3 and C5 but not of C2, in normal serum. These decreases in complement activity depended on the concentration of hydrogen peroxide added to the serum. Immunoelectrophoretic analysis of hydrogen peroxide-treated serum showed that C3 and C5 proteins were activated. Complement degradation products C3a and C5a were produced in normal serum treated with hydrogen peroxide, and 20 mM EDTA abolished C3a and C5a production in hydrogen peroxide-treated serum but 20 mM Mg-EGTA did not. Catalase completely abolished and dimethylsulphoxide and D-mannitol, hydroxyl radical scavengers, partially inhibited the hydrogen peroxide-mediated complement activation. Hypochlorite, incubated with normal serum, significantly inhibited serum haemolytic activity, and sodium thiosulphate, a reducing agent, abolished the effect of hypochlorite. Normal serum incubated with activated neutrophils showed neutrophil chemotactic activity and decreased serum haemolytic activity, and the addition of catalase or methionine (5 mM) completely abolished the effects of activated neutrophils. These results suggest that hydrogen peroxide activates complement via an alternative pathway of complement activation and that hydroxyl radicals and other hydrogen peroxide-related species such as hypochlorite are most likely involved in hydrogen peroxide-mediated complement activation. Complement activation by oxygen radicals produced by activated neutrophils may be one of the mechanisms by which complement is activated in human immune complex diseases.
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PMID:Activation of complement in normal serum by hydrogen peroxide and hydrogen peroxide-related oxygen radicals produced by activated neutrophils. 132 92

In order to better understand the enhancing effects of lowered oxygen (O2) tension on the growth in vitro of granulocyte-macrophage progenitor cells (CFU-GM), the effects of oxidizing species derived from molecular O2 were assessed on CFU-GM. Low density or nonadherent low density normal human bone marrow cells were plated at ambient (20%) or lowered (5%) O2 tension in the presence of a source of colony stimulating factors, and in the absence or presence of superoxide dismutase, catalase, glucose oxidase or horseradish peroxidase, alone or in various combinations. Enhanced colony and cluster formation of CFU-GM was noted when low density cells were grown at 5% O2, or when cells were grown at 20% O2 in the presence of superoxide dismutase or glucose oxidase. Both of these enzymes are capable of generating hydrogen peroxide (H2O2), although by different mechanisms. Low concentrations of glucose oxidase resulted in increased formation of colonies and clusters, but higher concentrations of glucose oxidase were inhibitory. Catalase, which converts H2O2 to H2O, had no effect by itself on cells growing at 20% O2, but it eliminated the superoxide dismutase and glucose oxidase enhancing effects. Catalase decreased colony formation of cells grown at 5% O2. Removal of adherent cells ablated the growth-enhancing effects noted at lowered (5%) O2 tension and also the superoxide dismutase and catalase effects at 20% or 5% O2. Horseradish peroxidase, which converts H2O2 to a more toxic oxidant, hypochlorite, had a suppressive effect on colony and cluster numbers and at 20% O2 converted the glucose oxidase effects from stimulatory to inhibitory. The results suggest that adherent cells and low concentrations of H2O2 may mediate growth-enhancing effects of CFU-GM seen at lowered (5%) O2 tension.
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PMID:The effects of oxidizing species derived from molecular oxygen on the proliferation in vitro of human granulocyte-macrophage progenitor cells. 273 50

The effect of hydrogen peroxide and hypochlorite on culture forms of Entamoeba histolytica trophozoites was examined by using two strains of E. histolytica, virulent (IP:0682:1) and nonvirulent (DKB). The amoebae were incubated with various concentrations of hydrogen peroxide and hypochlorite, and their viability was determined at different times after incubation. When the viability of the virulent and nonvirulent strains was compared to different oxidant strengths, it became apparent that the virulent strain was less susceptible than the nonvirulent one to the cytotoxic effect of hydrogen peroxide and hypochlorite. Our studies further showed that the toxic effect was both time and dose dependent. To confirm that the killing of amoebae in this system was associated with the presence of hydrogen peroxide, amoebae were incubated with hydrogen peroxide and catalase. Catalase reduced the killing effect of hydrogen peroxide to the control level. These data confirmed previous observations of the susceptibility of amoebic trophozoites to hydrogen peroxide and also demonstrated susceptibility to hypochlorite.
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PMID:Susceptibility of Entamoeba histolytica to oxidants. 286 45

Previously we have shown that human neutrophils treated with conditioned medium from phytohemagglutinin-stimulated mononuclear leukocytes (sCM) in the presence of antisera have amoebicidal properties for Naegleria fowleri, a pathogenic free-living amoeba. The data now presented show that neutrophils which lack myeloperoxidase (MPO) but have a normal oxygen-dependent respiratory burst could not be altered by sCM to express the amoebicidal activity. Catalase inhibited this amoebicidal activity of sCM-treated neutrophils. Various components and products of the neutrophils were examined for effects on naegleriae. A granule extract was found to have no effect at concentrations up to 100-fold that which killed Salmonella minnesota R595. Hydrogen peroxide appeared to have little effect even at 100 microM. However, in the presence of MPO, H2O2 was amoebicidal at 2.5 microM. The generation of amoebicidal activity required the presence of chloride ions. Azide inhibited the effects of the MPO-H2O2-Cl- system. Arginine, a scavenger of hypochlorite, significantly depressed the ability of sCM-treated neutrophils to kill amoebae and also prevented the amoebicidal properties of the MPO-H2O2-halide system. These results suggest that the MPO-H2O2-halide system is important in the killing of naegleriae by sCM-treated neutrophils and that hypochlorite may be the amoebicidal agent.
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PMID:Role of myeloperoxidase in the killing of Naegleria fowleri by lymphokine-altered human neutrophils. 303 97

Normal human monocytes were induced to lyse nonsensitized target cells when triggered by precipitating immune complexes (IC) or soluble heat-aggregated IgG (HAIgG). Catalase, azide, cyanide and three aminoacids employed as quenchers of ClO, significantly inhibited this nonspecific cytotoxicity (NSC), suggesting an important role for the myeloperoxidase (MPO) system. However, HO and/or 1O2 may also be involved in the lysis, since certain scavengers of these species such as mannitol, benzoate, ethanol and histidine, as well as superoxide dismutase (SOD), partially inhibited NSC. Moreover, cyanide and azide were unable to completely abrogate this lytic activity. When NSC was compared to antibody dependent cellular cytotoxicity (ADCC), it was found that neither catalase nor oxygen-species scavengers affected ADCC while azide and cyanide significantly enhanced it. Antibody-coated target cells were also destroyed by IC-triggered monocytes. However, kinetic analysis and studies on the capacity of catalase to inhibit the lysis demonstrated that it was mediated through a NSC-like mechanism. The cytotoxic system described in this report offers a suitable model to study in vitro alternative lytic mechanisms triggered through monocyte receptors for the Fc portion of IgG (Fc gamma R).
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PMID:The role of reactive oxygen intermediates in nonspecific monocyte cytotoxicity induced by immune complexes. 303 42

Escherichia coli can respond to gradients of specific compounds, moving up gradients of attractants and down gradients of repellents. Stimulated phagocytic leukocytes produce H2O2, OCl-, and N-chlorotaurine in a response termed the respiratory burst. E. coli is actively repelled by these compounds. Catalase in the suspending medium eliminated the effect of H2O2. Repulsion by H2O2 could be demonstrated with 1 microM H2O2, which is far below the level that caused overt toxicity. Strains with defects in the biosynthesis of glutathione or lacking hydroperoxidases I and II retained this response to H2O2, and 2.0 mM CN- did not interfere with it. Mutants with defects in any one of the four known methyl-accepting chemotaxis proteins also retained the ability to respond to H2O2, but a "gutted" mutant that was deleted for all four methyl-accepting chemotaxis proteins, as well as for CheA, CheW, CheR, CheB, CheY, and CheZ, did not respond to H2O2. Hypochlorite and N-chlorotaurine were also strongly repellent. Chemotaxis down gradients of H2O2, OCl-, and N-chlorotaurine may contribute to the survival of commensal or pathogenic microorganisms.
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PMID:Escherichia coli exhibits negative chemotaxis in gradients of hydrogen peroxide, hypochlorite, and N-chlorotaurine: products of the respiratory burst of phagocytic cells. 864 18

In this paper, the quenching of hydrogen peroxide by catalase, sodium hypochlorite, sodium thiosulfate and sodium sulfite, prior to UFC testing, was investigated. Sodium hypochlorite, sodium thiosulfate and sodium sulfite were found to be unsuitable for quenching H2O2 residuals because the procedures are time-consuming and complicated in that they require potentially multiple measurements of the peroxide and chlorine residuals. In contrast, quenching of peroxide with catalase is a simple procedure. Catalase doses of less than 0.2 mg/L were found to have no impact on DBP (TTHM, HAA and aldehyde) formation in the UFC test, and the time that was needed to quench 100 mg/L peroxide (room temperature, pH 8.3) was less than 10 min. In addition, peroxide was found to react with DPD reagents that are used to measure chlorine residuals, a phenomenon that may lead to falsely high chlorine residuals in the UFC test.
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PMID:Optimal methods for quenching H2O2 residuals prior to UFC testing. 1286 37

Oxidative stress plays an important role in the pathogenesis of diabetic complications, and we investigated the effect of superoxide dismutase (SOD) mimetic, tempol, in diabetic nephropathy. Streptozotocin-induced diabetic rats were treated with tempol from 2 weeks until 8 weeks. The expression of NADPH oxidase, catalase, and myeloperoxidase (MPO), superoxide dismutase activity, and production of peroxide and hypochlorite were evaluated. Tempol treatment prevented the increase in NADPH oxidase and peroxide production in the glomeruli of diabetic rat. Catalase was decreased without change in SOD activity, and MPO was enhanced in the kidney of diabetic rats. Tempol treatment stimulated SOD activity and increased the conversion of superoxide to hydrogen peroxide, and hydrogen peroxide on its hand was converted to hypochlorite by the increased MPO. The reduction of peroxide by tempol was followed by the decrease in TGF-beta and mesangial matrix expansion. However, tempol did not reduce hypochlorite or urinary protein excretion. In conclusion, tempol inhibited glomerular matrix expansion via suppression of peroxide production and TGF-beta, but it failed to reduce proteinuria, probably due to the increased hypochlorite production in diabetic nephropathy.
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PMID:Double-edged action of SOD mimetic in diabetic nephropathy. 1726 58

This study was carried out in order to investigate the ability of tissues of Argania spinosa (L.) to undergo unlimited cell divisions by triggering their proliferative potential via callogenesis. Axenic cultures were efficiently established using axillary buds cultured on half-strength Murashige and Skoog (MS) medium after 20min of surface sterilization with sodium hypochlorite 6% (v/v). The highest callus rate was achieved with 1.0mgL-1 of naphthaleneacetic acid (NAA) and 1.0mgL-1 of 2,4-dichlorophenoxyacetic acid (2,4D) or similarly with 0.01mgL-1 of 6-benzylaminopurine (BAP) and 1.0mgL-1 of 2,4D at pH of 5.8, under dark conditions. The results of this study show also a significant increase in the callus's antioxidant power under abiotic pressure induced by NaCl. Catalase (CAT), peroxidase (PO), and superoxide dismutase (SOD) activities were significantly triggered, which protected the cells from the stimulated oxidative stress, under hydrogen peroxide (H2O2) significant release. This reaction favors subsequently the tissue recover process linked to the low abundance of polyphenol oxidase (PPO) activity and malondialdehyde (MDA) content. This work proves the efficiency of salt stress in boosting the argan cell's antioxidant status, which could be commercially applied in the field of cells regenerative therapy.
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PMID:Uprising the antioxidant power of Argania spinosa L. callus through abiotic elicitation. 3059 94