Free radicals and inflammation. Protection of phagocytosine leukocytes by superoxide dismutase.

Salin, Marvin L.; McCord, Joe M.

doi:10.1172/jci108208

Cited by 266 publications

(78 citation statements)

References 14 publications

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“…Taken together with the enhanced recovery of H202 from cells exposed to SOD this observation strongly suggests that phagocytizing granulocytes generate more 02. than can be accounted for by spontaneous dismutation to H202. Potential pathways for 02. utilization other than dismutation include oxygenation reactions involving unsaturated lipids either in the bacteria or the leukocytes themselves (5), competing reduction reactions, and in the presence of H202, its consumption in the generation of singlet oxygen and hydroxyl radicals (21)(22)(23)(24)(25). The relative importance of these other reactions to the microbicidal and inflammatory capabilities of the granulocyte remain to be determined, but our studies provide quantitative support for their existence.…”

Section: Discussionmentioning

confidence: 73%

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H2O2 Release from Human Granulocytes during Phagocytosis

Root¹,

Metcalf²

1977

J. Clin. Invest.

485

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A B S T R A C T Normal and cytochalasin B-treated human granulocytes have been studied to determine some of the interrelationships between phagocytosisinduced respiration and superoxide and hydrogen peroxide formation and release into the extracellular medium by intact cells. By using the scopoletin fluorescent assay to continuously monitor extracellular hydrogen peroxide concentrations during contact of cells with opsonized staphylococci, it was demonstrated that the superoxide scavengers ferricytochrome c and nitroblue tetrazolium significantly reduced the amount of H202 released with time from normal cells but did not abolish it. This inhibitory effect was reversed by the simultaneous addition of superoxide dismutase (SOD), whereas the addition of SOD alone increased the amount of detectable H202 in the medium. The addition of sodium azide markedly inhibited myeloperoxidase-H202-dependent protein iodination and more than doubled H202 release, including the residual amount remaining after exposure of the cells to ferricytochrome c, suggesting its origin from an intracellular pool shared by several pathways for H202 catabolism. When cells were pretreated with cytochalasin B and opsonized bacteria added, reduced oxygen consumption was observed, but this was in parallel to a reduction in specific binding of organisms to the cells when compared to normal. Under the influence of inhibited phagosome formation by cytochalasin B, the cells released an increased amount of superoxide and peroxide into the extracellular medium relative to oxygen consumption, and all detectable peroxide release could be inhibited by the addition of ferricytochrome c. Decreased H202 production in the presence of this compound could not be ascribed to diminished bacterial binding, decreased oxidase activity, or increased H202 catabolism and was reversed by the simultaneous addition of SOD. Furthermore, SOD and ferricytochrome c had similar effects on another H202-dependent reaction, protein iodination, in both normal and cytochalasin B cells. When oxygen consumption, 02., and H202 release were compared in the presence of azide under identical incubation conditions, the molar relationships for normal cells were 1.00:0.34:0.51 and for cytochalasin B-treated cells 1.00:0.99:0.40, respectively. Nonopsonized, or opsonized but disrupted, bacteria did not stimulate any of these metabolic functions.The results indicate that with normal cells approximately 50% of H202 released during phagocytosis is derived directly from 02: by dismutation, the remainder appearing from an (intra)cellular source shared by azide-inhibitable heme enzymes. With cytochalasin B treatment the evidence is consistent with the derivation of all H202 from an 02: precursor which is released from the cell surface. Furthermore, when activated by phagocytic particle

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Section: Discussionmentioning

confidence: 73%

“…Furthermore, debate exists as to whether H202 (4,7,17,18) or 02. (3,5,6,(19)(20)(21) is primarily involved in the effector mechanism of oxygen-dependent killing or whether both might play a role through the generation of other active oxygen compounds such as the hydroxyl radical and singlet oxygen (4,(21)(22)(23)(24)(25).…”

Section: Introductionmentioning

confidence: 99%

H2O2 Release from Human Granulocytes during Phagocytosis

Root¹,

Metcalf²

1977

J. Clin. Invest.

485

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“…Metabolism of oxygen is greatly responsible for producing superoxide and if not controlled causes many types of cell damage [74]. SOD is a metalloenzyme that exert protection in cells exposed to oxygen.…”

Section: Discussionmentioning

confidence: 99%

Analyzing Nootropic Effect of <i>Phyllanthus reticulatus</i> Poir. on Cognitive Functions, Brain Antioxidant Enzymes and Acetylcholinesterase Activity against Aluminium-Induced Alzheimer’s Model in Rats: Applicable for Controlling the Risk Factors of Alzheimer’s Disease

Mamun¹,

Iqbal²,

Islam³

et al. 2016

AAD

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“…Although the primary role of these processes is considered to be the killing of ingested microorganisms within the phagocytic vacuole, leakage or secretion of toxic agents into the extracellular fluid can occur. Thus, the metabolic burst results in the formation of several reactive species of partially reduced oxygen, including superoxide anion, hydrogen peroxide (H202), and hydroxyl radical (2,3), and some of these agents have been detected in the extracellular fluid adjacent to the activated PMN (4)(5)(6)(7)(8). Degranulation can result in the emptying of granule enzymes, such as acid hydrolases and myeloperoxidase, into the extracellular fluid (9)(10)(11)(12)(13).…”

Section: Introductionmentioning

confidence: 99%

Myeloperoxidase-Mediated Platelet Release Reaction

Clark¹,

Klebanoff²

1979

J. Clin. Invest.

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A B S T R A C T The ability of the neutrophil myeloperoxidase-hydrogen peroxide-halide system to induce the release of human platelet constituents was examined. Both resulted in a small, although significant, release ofboth serotonin and adenine, suggesting some platelet lysis. Substantial release of these markers was observed only with increased H202 concentrations (>0.1 mM) or prolonged incubation (1-2 h).Serotonin release by H202 was markedly enhanced by the addition ofmyeloperoxidase and a halide. Under these conditions, there was a predominance of release of serotonin (50%) vs. adenine (13%), suggesting, in part, a nonlytic mechanism. Serotonin release by the complete peroxidase system was rapid, reaching maximal levels in 2-5 min, and was active at H202 concentrations as low as 10 ,uM. It was blocked by agents which inhibit peroxidase (azide, cyanide), degrade H202 (catalase), chelate Mg2+ (EDTA, but not EGTA), or inhibit platelet metabolic activity (dinitrophenol, deoxyglucose).These results suggest that the myeloperoxidase system initiates the release of platelet constituents primarily by a nonlytic process analogous to the platelet release reaction. Because components of the peroxidase system (myeloperoxidase, H202) are secreted by activated neutrophils, the reactions described here may have implications for neutrophilplatelet interaction in sites of thrombus formation.Portions of this work have appeared in abstract form: Clin.

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Free radicals and inflammation. Protection of phagocytosine leukocytes by superoxide dismutase.

Cited by 266 publications

References 14 publications

H2O2 Release from Human Granulocytes during Phagocytosis

H2O2 Release from Human Granulocytes during Phagocytosis

Analyzing Nootropic Effect of <i>Phyllanthus reticulatus</i> Poir. on Cognitive Functions, Brain Antioxidant Enzymes and Acetylcholinesterase Activity against Aluminium-Induced Alzheimer’s Model in Rats: Applicable for Controlling the Risk Factors of Alzheimer’s Disease

Myeloperoxidase-Mediated Platelet Release Reaction

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Free radicals and inflammation. Protection of phagocytosine leukocytes by superoxide dismutase.

Cited by 266 publications

References 14 publications

H2O2 Release from Human Granulocytes during Phagocytosis

H2O2 Release from Human Granulocytes during Phagocytosis

Analyzing Nootropic Effect of &lt;i&gt;Phyllanthus reticulatus&lt;/i&gt; Poir. on Cognitive Functions, Brain Antioxidant Enzymes and Acetylcholinesterase Activity against Aluminium-Induced Alzheimer’s Model in Rats: Applicable for Controlling the Risk Factors of Alzheimer’s Disease

Myeloperoxidase-Mediated Platelet Release Reaction

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Product

Resources

About

Analyzing Nootropic Effect of <i>Phyllanthus reticulatus</i> Poir. on Cognitive Functions, Brain Antioxidant Enzymes and Acetylcholinesterase Activity against Aluminium-Induced Alzheimer’s Model in Rats: Applicable for Controlling the Risk Factors of Alzheimer’s Disease