Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:1.11.1.7 (peroxidase)
65,474 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The interaction of human polymorphonuclear neutrophilic leukocytes (neutrophils) with interleukin-1 (IL-1) resulted in a time- and concentration-dependent, selective, release of azurophil (myeloperoxidase, lysozyme) and specific (lysozyme, vitamin B12-binding protein) granule constituents. Myeloperoxidase (MPO) and lysozyme secretion was markedly attenuated if neutrophils were not exposed to cytochalasin B (CB) prior to contact with IL-1. Degranulation was significantly enhanced in the presence of extracellular calcium. IL-1-elicited granule exocytosis was inhibited by the intracellular calcium antagonist, 8-(N,N-diethylamino)-octyl-(3,4,5-trimethoxy) benzoate hydrochloride (TMB-8), a calmodulin antagonist, trifluoperazine (TFP), and an anion channel blocker, 4,4'-diisothiocyano-2,2'-disulfonic acid stilbene (DIDS). An evaluation of the role of arachidonic acid metabolites in IL-1-induced neutrophil activation revealed a suppressive effect on enzyme release exerted by the lipoxygenase inhibitors, piriprost potassium (6,9,deepoxy-6,9-(phenylimino)-delta 6,8 -prostaglandin I1, U-60,257B) and NDGA (nordihydroguaiaretic acid), and a cyclooxygenase/lipoxygenase inhibitor, ETYA (5,8,11,14-eicosatetraynoic acid). These data describe the characteristics of IL-1 as a human neutrophil secretagogue, and enhance our insight into the mechanism of inflammatory cell activation with this monokine.
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PMID:Interleukin-1 stimulates granule exocytosis from human neutrophils. 242 Jul 32

Singlet oxygen (1 delta g) is a highly reactive, short-lived intermediate which readily oxidizes a variety of biological molecules. The biochemical production of singlet oxygen has been proposed to contribute to the destructive effects seen in a number of biological processes. Several model biochemical systems have been shown to produce singlet oxygen. These systems include the peroxidase-catalyzed oxidations of halide ions, the peroxidase-catalyzed oxidations of indole-3-acetic acid, the lipoxygenase-catalyzed oxidation of unsaturated long chain fatty acids and the bleomycin-catalyzed decomposition of hydroperoxides. Results from these model systems should not be uncritically extrapolated to living systems. Recently, however, an intact cell, the human eosinophil, was shown to generate detectable amounts of singlet oxygen. This result suggests that singlet oxygen may be shown to be a significant biochemical intermediate in a few biological processes.
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PMID:Singlet oxygen production by biological systems. 247 24

We recently demonstrated activation of 5-lipoxygenase activity in human polymorphonuclear leukocytes (PMN) on preincubation of the cells with glutathione-depleting agents, namely 1-chloro-2,4-dinitrobenzene (Dnp-C1) and azodicarboxylic acid bis[dimethylamide] (diamide). In this paper we show that Dnp-C1, but not diamide, impairs the reduction of added organic peroxides in whole PMN. Also, since co-incubation of fatty acid hydroperoxides with arachidonate caused activation of 5-lipoxygenase, we propose that Dnp-C1 increases the peroxide level in PMN which is required for the onset of lipoxygenase activity. This could be substantiated in PMN homogenates by a glutathione-dependent depression of arachidonate 5-lipoxygenation. At higher arachidonate concentrations and in the presence of Ca2+ the glutathione effect was not observed but additional glutathione peroxidase also blocked this maximally stimulated 5-lipoxygenase. Together with other experiments, it became obvious that the formation of leukotrienes, but also of 15-lipoxygenase products, requires a sharply defined threshold level of fatty acid hydroperoxides which are generated by the lipoxygenases and counteracted by glutathione-dependent peroxidase(s). Dnp-C1 influences this equilibrium by removing glutathione and thereby inhibiting glutathione-dependent peroxidase activity. From our data we conclude that it is the physiological function of the peroxidase activity in PMN to determine an efficiently regulated threshold level of hydroperoxide products, below which no activation of 5-lipoxygenase or 15-lipoxygenase can occur.
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PMID:Involvement of glutathione peroxidase activity in the stimulation of 5-lipoxygenase activity by glutathione-depleting agents in human polymorphonuclear leukocytes. 249 78

Platelets administered 1-chloro-2,4-dinitrobenzene to deplete intracellular glutathione (GSH) and inhibit GSH-peroxidase responded with irreversible aggregation to low doses of arachidonic acid (AA) more rapidly than control cells. This increase in sensitivity was correlated to inhibition of GSH-peroxidase, and not with the depletion of GSH. Addition of hydrogen peroxide, 15-hydroperoxyeicosatetraenoic acid, or inhibition of the lipoxygenase metabolic pathway by 4,7,10,13-eicosatetraynoic acid also induced a hypersensitive aggregation response to AA. These results suggest that the three modes of treatment share a common mechanism of increasing AA metabolism to biologically active prostaglandins and thromboxane A2 through alterations in cyclooxygenase kinetics and available enzyme substrate.
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PMID:Platelet hypersensitivity induced by 1-chloro-2, 4-dinitrobenzene, hydroperoxides and inhibition of lipoxygenase. 249 41

Selective removal of intracellular glutathione (GSH) and inhibition of the GSH-dependent peroxidase (GSH-Px) by 1-chloro-2,4-dinitrobenzene (CDNB) was used to evaluate the role of GSH and GSH-Px in arachidonic acid (AA) metabolism in human platelets. Although total conversion of AA through the lipoxygenase pathway is lowered by GSH depletion, significant 12-HETE formation was observed suggesting that GSH and GSH-Px are not required for the generation of 12-HETE in human platelets. Prolonged treatment of platelets with CDNB (2 h) completely destroyed GSH-Px activity creating a model in which the effects of GSH alone could be determined. Platelet homogenates replenished with GSH, but lacking GSH-Px activity converted significantly higher amounts of AA to 12-HPETE and 12-HETE than control. Platelet cytosolic metabolism of 15-HPETE to 15-HETE decreased after CDNB, while the membrane metabolism remained similar to control due to high GSH-independent peroxidase activity associated with the membranes. These results indicate that GSH and GSH-Px function to enhance lipoxygenase activity, rather than catalyse the reduction of 12-HPETE to 12-HETE.
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PMID:Role of glutathione and glutathione peroxidase in human platelet arachidonic acid metabolism. 250 28

Soybean lipoxygenase shows a secondary peroxidase/oxidase activity: The aerobic reaction with isobutanal, enhanced by hydrogen peroxide as a cosubstrate, yields acetone, exhibits chemiluminescence and consumes oxygen (phi cl = 1.3 x 10(-9) photons/O2 molecule consumed). 9,10-Dibromoanthracene-2-sulfonate increases the photoemission (kET tau 0 = 2 x 10(4) M-1; phi cl = 0.9 x 10(-7) photons/O2), whereas it is diminished by sorbate, tryptophan, 2-methyl-1,4-naphthoquinone, glutathione, and superoxide dismutase. In the presence of hydrogen peroxide the lipoxygenase reaction with glutathione yields yet another excited state. From the well-known reactions promoted by horseradish-peroxidase, these features are concluded to indicate the novel activity of soybean lipoxygenase. With isobutanal as a substrate lipoxygenase acts as an oxidase and as a peroxidase. The mechanism suggested leads to photoemissive triplet excited acetone as expected from the cleavage of an intermediate dioxetane.
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PMID:The peroxidase/oxidase activity of soybean lipoxygenase--I. Triplet excited carbonyls from the reaction with isobutanal and the effect of glutathione. 250 78

During the aerobic reaction of soybean lipoxygenase with polyunsaturated fatty acids (linoleic, linolenic, and arachidonic acid) oxygen uptake is followed by excited carbonyl photoemission. The chemiluminescence yield of phi cl = 10(-10) photons/O2 molecule consumed is enhanced 2-3 orders of magnitude by the carbonyl sensitizers 9,10-dibromo-anthracene-2-sulfonate (kET tau 0 = 10(4) M-1; phi cl = 10(-8) photons/O2) and chlorophyll-a (kET tau 0 = 10(6) M-1; phi cl = 10(-7) photons/O2), respectively. alpha,beta-Saturated triplet excited carbonyls as from 1,2-dioxetane cleavage are discussed to arise from a secondary peroxidase/oxidase reaction with aldehydes formed in the course of enzymic lipid peroxidation. When 1 mM glutathione is added to the aerobic lipoxygenase/arachidonate reaction, carbonyl emission (375-455 nm) is replaced by intense red bands (630-645 nm and 695-715 nm) resembling the characteristic spectrum of (1 delta g)O2-singlet oxygen dimol-emission. The quantum yield (phi cl = 10(-8) photons/O2) remains unaffected by chlorophyll indicating that the red emission is independent of excited carbonyls. The effect of GSH is attributed to dioxetane interception and subsequent glutathione peroxidation generating 1O2 by electron transfer from the superoxide anion radical to a peroxysulfenyl radical.
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PMID:The peroxidase/oxidase activity of soybean lipoxygenase--II. Triplet carbonyls and red photoemission during polyunsaturated fatty acid and glutathione oxidation. 250 79

It was shown in several cell types that the dual lipoxygenase and cyclooxygenase inhibitor eicosatetraynoic acid but not the cyclooxygenase inhibitor acetylsalicylic acid suppressed luminol-dependent chemiluminescence. Since lipoxygenase is known to generate chemiluminescence in vitro, these observations were interpreted as evidence for a direct contribution of the lipoxygenase pathway to light emission in intact cells. We have investigated a possible contribution of the lipoxygenase to the chemiluminescence of horse eosinophils by directly comparing the formation of the byproduct chemiluminescence with the formation of stable end-products of the lipoxygenase pathway, leukotrienes and HETEs. Azide as well as eicosatetraynoic acid almost completely inhibited chemiluminescence stimulated by the calcium ionophore A23187 but had less effect on the formation of leukotrienes. The tumour-promoting ester, phorbol myristate acetate, stimulated chemiluminescence in an azide- and eicosatetraynoic acid-sensitive manner and failed to evoke the production of leukotrienes. Azide, but also eicosatetraynoic acid inhibited the luminol-dependent chemiluminescence generated by isolated eosinophil peroxidase in the presence of H2O2. Our results argue against a direct role of the lipoxygenase pathway in the generation of light in horse eosinophilic leukocytes but do not exclude that product(s) of this pathway may be involved in stimulus-response coupling.
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PMID:The lipoxygenase pathway and chemiluminescence in horse eosinophilic leukocytes. 250 36

The interaction of H2O2 with soyabean lipoxygenase was investigated in the presence of linoleic acid. Dioxygenase activity was significantly higher at pH 9.0 than at pH 6.0. H2O2 at concentrations less than 1.0 nM stimulated linoleic acid oxidation synergistically and the magnitude of synergism was higher at pH 9.0. Linoleic acid dependent peroxidase activity towards benzidine, guaiacol, tetramethylbenzidine (TMBD) and tetramethylphenylenediamine (TMPD) was higher at pH 9.0, whereas pyrogallol and ABTS oxidation rates were higher at pH 6.0. H2O2 supported oxidation of benzidine, guaiacol, pyrogallol and ABTS was higher at pH 6.0, whereas TMPD, TMBD exhibited higher oxidation rates at pH 9.0. H2O2 in the presence of linoleic acid produced synergism in xenobotic metabolism and depending upon the substrate in question upto 11-fold increase in oxidation rate was noted.
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PMID:Dioxygenase and peroxidase activities of soybean lipoxygenase: synergistic interaction between linoleic acid and hydrogen peroxide. 251 25

Colitis was induced in rats by intrarectal administration of trinitrobenzene sulfonic acid (80 mg/kg, in 30% ethanol). An acute inflammation with ulcers and neutrophil infiltration developed that evolved into a chronic inflammation and luminal narrowing with attendant smooth muscle hypertrophy. We assessed the effects of 16,16-dimethyl prostaglandin E2, administered either before or after trinitrobenzene sulfonic acid, on the development of inflammation. Inflammation was assessed by gross appearance using a grading scale (0-4) and by histology. The number of neutrophils present in inflamed colonic tissue was quantitated by the myeloperoxidase assay. The production of lipoxygenase products was monitored by incubation of colonic specimens with [14C]arachidonic acid and separation of the products by thin-layer chromatography and high-pressure liquid chromatography. Levels of leukotriene B4 were measured in tissue extracts by high-pressure liquid chromatography and ultraviolet absorbance. Eicosanoid production was also assayed by incubating colonic specimens and assaying the media for prostaglandin E2, leukotriene B4, and leukotriene C4 by radioimmunoassay. Trinitrobenzene sulfonic acid treatment resulted in a greatly increased amount of leukotriene B4 in the media. Treatment with 16,16-dimethyl prostaglandin E2 before administration of trinitrobenzene sulfonic acid resulted in a lower inflammation index, lower myeloperoxidase activity, and decreased production of leukotriene B4. Administration of 16,16-dimethyl prostaglandin E2 24 h after administration of trinitrobenzene sulfonic acid was also effective in reducing the inflammatory response. Treatment with 16,16-dimethyl prostaglandin E2 also prevented the development of long-term architectural changes 3 wk after administration of trinitrobenzene sulfonic acid. Rectal administration of dimethyl prostaglandin E2 also diminished the colitis induced by direct injection of trinitrobenzene sulfonic acid into the colonic wall.
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PMID:Treatment with 16,16'-dimethyl prostaglandin E2 before and after induction of colitis with trinitrobenzenesulfonic acid in rats decreases inflammation. 279 68


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