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 Fc gamma receptor of rabbit alveolar macrophages was purified by affinity chromatography by using rabbit gamma-globulin (Rab gamma G) coupled to Sepharose. Macrophage preparations were efficiently labeled with 125I by using a modified lactoperoxidase method. After incubation of NP-40 cell lysates with Rab gamma G-Sepharose, elution at 4 degrees C with 0.5 N acetic acid containing 1% NP-40 and rapid neutralization allowed recovery of active Fc gamma receptor. Purified Fc gamma receptor retained its ligand-binding activity, since approximately 41 to 72% of labeled material specifically rebound to Rab gamma G-Sepharose. Active receptor also rebound to human IgG- and rat IgG-sepharose. Active Fc gamma receptor did not bind to Sepharose coupled to rabbit Fab, rabbit F(ab)'2 or human F(ab)'2 fragments, nor to Sepharose coupled to chicken IgG. Analysis of Fc gamma receptor by SDS polyacrylamide gels demonstrated a broad peak of radioactivity in the apparent m.w. range of 50,000 to 70,000 in 5.6% acrylamide gels and 35,000 to 55,000 in 9% gels. Labeled receptor with similar structural characteristics and ligand-binding activity was also obtained from highly purified adherent cell populations and from macrophages biosynthetically-labeled with [14C]glucosamine in culture.
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PMID:Purification of Fc gamma receptor from rabbit alveolar macrophages that retains ligand-binding activity. 737 49

The synthesis of the heterobifunctional cross-linking reagent 2-nitro-4-azidophenylsulfenyl chloride (NAPSCl) is described. This reagent can be used to specifically attach a photoactivatable nitrophenyl azide to tryptophan-containing polypeptides and proteins lacking sulfhydryl groups. The sulfenyl chloride group of NAPSCl reacts with the indole ring of tryptophan following second-order reaction kinetics in 50-100% acetic acid. The labeled product can be effectively photolyzed at wavelengths above 300 nm. The reaction of glucagon, a peptide hormone containing a single tryptophan residue at position 25 and no cysteine, with NAPSCl gave one major product, the photosensitive derivative glucagon-NAPS. The structure and properties of the purified derivative were established by amino acid analysis, absorption spectroscopy, and photolysis. Only the tryptophan residue of this derivative was modified. The photosensitive glucagon was shown to activate the adenylate cyclase of hepatocyte plasma membranes to the same extent as the native hormone at equimolar concentrations. Glucagon-NAPS could be radiolabeled by the lactoperoxidase-catalyzed iodination of the peptide. A glucagon-specific antibody bound both radiolabeled glucagon and glucagon-NAPS peptides. The covalent labeling of protein molecules with radiolabeled glucagon-NAPS peptide upon photolysis was demonstrated. Glucagon-NAPS can be used as an effective photoaffinity probe for labeling the glucagon receptor site in plasma membranes of target cells.
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PMID:Synthesis and characterization of a heterobifunctional photoaffinity reagent for modification of tryptophan residues and its application to the preparation of a photoreactive glucagon derivative. 742 13

The horseradish peroxidase catalyzed aerobic oxidation of the auxin indole-3-acetic acid generates triplet indole-3-aldehyde in high yield. The excited species is quenched by oxygen with formation of singlet oxygen, which is responsible for the observed photon emission and can be trapped by suitable agents. tRNA dramatically enhances the emission as a result of energy transfer from triplet indole-3-aldehyde to a 4-thiouridine group in tRNA. Triplet indole-3-aldehyde also adds covalently to tRNA. The results provide a possible mechanism for the auxin-tRNA interaction in vivo.
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PMID:Excited indole-3-aldehyde from the peroxidase-catalyzed aerobic oxidation of indole-3-acetic acid. Reaction with and energy transfer to transfer ribonucleic acid. 744 69

Fc gamma-binding macromolecules were isolated from 2 murine macrophage-like cell lines by affinity chromatography using various immunoglobulins coupled to Sepharose. P388D1 and J744.2 cells were radiolabeled with 125I using a modified lactoperoxidase method, washed cells were solubilized using NP-40, and the solubilized cell lysates were incubated at 4 degrees C with immunoadsorbents. Fc gamma receptor-like material was obtained from the IgG-Sepharose columns by elution at 4 degrees C with 0.5 N acetic acid containing 1% NP-40 into buffer for neutralization. Purified material thus obtained retained its ligand-binding activity, since approximately 30 to 60% rebound to IgG-Sepharose. Upon analysis by SDS polyacrylamide gel electrophoresis, putative Fc gamma receptor had an apparent m.w. of 50 to 65,000. Neither a comparable SDS-PAGE band nor receptor activity was isolated from a 3rd murine cell line, which lacks the Fc gamma receptor. Putative receptor obtained by elution from IgG2a-Sepharose rebound equally well to IgG2a-, IgG1- and IgG2b-Sepharose, but did not rebind to IgG3-, F(ab')2-, or BSA-Sepharose. Similarly, Fc gamma-binding macromolecules eluted from IgG2b-Sepharose rebound only to IgG2b-, IgG2a- and IgG1-Sepharose rebound only to IgG2b-, IgG2a- and IgG1-Sepharose. The rebinding of either receptor preparation was inhibited in a dose-dependent manner by both monomeric IgG2a and monomeric IgG2b, and myeloma protein from each subclass inhibited to the same extent. Therefore, the mouse Fc gamma receptor in its isolated state does not appear to discriminate between monomeric IgG2a and IgG2b.
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PMID:Characterization of ligand-binding activity of isolated murine Fc gamma receptor. 745 92

Enhanced nitric oxide (NO) generation by stimulated NO synthase (NOS) activity may, through its oxidative metabolism contribute to tissue injury in experimental colitis. In this study the possible amelioration of experimental colitis by NG-nitro-L-arginine methyl ester (L-NAME), an inhibitor of NOS activity, was evaluated. Colitis was induced in rats by intracolonic administration of 30 mg trinitrobenzene sulphonic acid (TNB) dissolved in 0.25 ml 50% ethanol or by flushing the colon of capsaicin pretreated rats with 2 ml of 5% acetic acid. In several experiments, L-NAME 0.1 mg/ml was added to the drinking water at the time of colitis induction with TNB or seven days before acetic acid treatment. Rats were killed at various time intervals after induction of colitis. A 10 cm distal colonic segment was isolated, weighed, lesion area measured, and explants organ cultured for 24 hours for determination of NO generation by the Greiss reaction. The rest of the mucosa was scraped for determination of myeloperoxidase and NOS activities and leukotriene generation. In TNB treated rats mean arterial pressure was also determined up to 72 hours after damage induction, with or without cotreatment with nitroprusside. L-NAME significantly decreased the extent of tissue injury in TNB treated rats. Seven days after TNB treatment lesion area was reduced by 55%, colonic weight by 37%, and myeloperoxidase and NOS activity by 59% and 42%, respectively. Acetic acid induced colitis in capsaicin pretreated rats was also significantly decreased by L-NAME. Twenty four hours after acetic acid treatment lesion area was reduced by 61%, colonic weight by 21% and NOS activity by 39%. Mean (SEM) arterial blood pressure in TNB+L-NAME treated rats was 37.6 (8.1) mm Hg higher than in TNB treated rats, an effect that was only partially abolished by nitroprusside. These results show that inhibition of NO synthesis by an L-arginine analogue significantly ameliorates the extent of tissue injury in two models of experimental colitis, an effect that is not due only to its vasoconstrictor properties. Modulation of NO generation may be a novel therapeutic approach in inflammatory bowel disease.
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PMID:Experimental colitis is ameliorated by inhibition of nitric oxide synthase activity. 867 8

The peroxidation of liposomes by a haem peroxidase and hydrogen peroxide in the presence of indole-3-acetic acid and derivatives was investigated. It was found that these compounds can accelerate the lipid peroxidation up to 65 fold and this is attributed to the formation of peroxyl radicals that may react with the lipids, possibly by hydrogen abstraction. The peroxyl radicals are formed by peroxidase-catalyzed oxidation of the enhancers to radical cations which undergo cleavage of the carbon-carbon bond on the side-chain to yield CO2 and carbon-centred radicals that rapidly add oxygen. In competition with decarboxylation, the radical cations deprotonate reversibly from the N1 position. Rates of decarboxylation, pka values and rate of reaction with the peroxidase compound I indicate consistent substituent effects which, however, can not be quantitatively related to the usual Hammett or Brown parameters. Assuming that the rate of decarboxylation of the radical cations taken is a measure of the electron density of the molecule (or radical), it is found that the efficiency of these compounds as enhancers of lipid peroxidation increases with increasing electron density, suggesting that, at least in the model system, the oxidation of the substrates is the limiting step in causing lipid peroxidation.
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PMID:Enhancement of lipid peroxidation by indole-3-acetic acid and derivatives: substituent effects. 758 24

TEMPOL, a cyclic nitroxide stable radical blocks biological damage by breaking chain reactions through termination reaction with free radicals, and by inhibiting the catalytic effect of transition metals. This study tested its protective effect on two models of experimental colitis as free radicals play an important part in their pathogenesis. TEMPOL was given intragastrically immediately after induction of colitis with acetic acid or trinitrobenzene sulphonic acid (TNB) and mucosal damage was assessed one, three, or seven days later. Cellular partition of TEMPOL was determined by electron paramagnetic resonance spectroscopy. In vitro experiments showed that TEMPOL immediately penetrates colonic mucosa and, following its intragastric administration, it persists in both gastric and colonic mucosa for several hours. Intragastric administration of TEMPOL, 0.5 g/kg/bw, immediately after intracaecal administration of 5% acetic acid significantly decreased mucosal lesion area, myeloperoxidase activity, and leukotriene B4 and C4 generation when assessed 24 hours after damage induction. Intragastric administration of TEMPOL, 0.5 g/kg/bw, immediately after intracolonic administration of 30 mg TNB in 0.25 ml 50% ethanol, and once daily thereafter, significantly decreased mucosal lesion area assessed after one, three, and seven days, having no effect on LTC4 generation and affecting colonic weight, myeloperoxidase activity, and LTB4 generation only sporadically. In conclusion, TNB and acetic acid induced colitis can be pharmacologically manipulated by TEMPOL. TEMPOL may be beneficial in the treatment or prevention of inflammatory bowel disease.
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PMID:A stable nitroxide radical effectively decreases mucosal damage in experimental colitis. 759 Apr 35

The transendothelial migration of leukocytes in many inflammatory responses is now believed to be dependent on the interaction of leukocyte and endothelial cell-derived adhesion molecules. To examine the role of intercellular adhesion molecule-1 (ICAM-1) in the development of inflammation in a rat model of colitis, we investigated the effects of antibodies to rat ICAM-1 given 24 hrs after inflammation was induced by acetic acid. Antibodies to rat ICAM-1 substantially ameliorated the inflammatory response as indicated by a reduction in gross inflammatory characteristics, tissue/body weight ratio, myeloperoxidase activity and superoxide levels. The results demonstrate that ICAM-1 plays an important role in the development of inflammatory bowel disease in rats. The use of antibodies to ICAM-1 to inhibit the adherence of leukocytes to endothelium, may be of potential therapeutic value in the treatment of inflammatory bowel disease in man.
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PMID:Antibodies to intercellular adhesion molecule-1 ameliorate the inflammatory response in acetic acid-induced inflammatory bowel disease. 761 34

The healing of acetic acid-induced gastric ulcer in rats and the effects of cimetidine and calcitonin were investigated with reference to the enzyme activity of both prolylhydroxylase and collagenase as related to histological findings. The rats were observed by endoscopy on the 3rd day after the subserosal injection of acetic acid; rats with ulcers were divided into three groups: non-treated, and cimetidine- and calcitonin-treated. The latter two groups were treated for 7 days. Prolylhydroxylase activity in active ulcers in the non-treated group was slightly higher on the 3rd day and significantly higher on the 10th day than the activity in control rats that had received subserosal injections of physiological saline solution on the respective days. In non-treated rats, the healed ulcer on the 10th day showed lower prolylhydroxylase activity than that in the active ulcer on the same day. Cimetidine did not affect prolylhydroxylase activity, but, with calcitonin, there was higher prolylhydroxylase activity in the healed than in the active ulcer, although the difference was not significant. Interstitial collagenase showed the highest activity on the 3rd day and decreased on the 10th day in non-treated rats. Collagenase activity was higher in the cimetidine-treated group, than that in the non-treated group, and numerous peroxidase-positive granulocytes were seen in the mucosa and submucosa. Calcitonin did not affect collagenase activity. The participation of both enzymes is indispensable in the healing process and the effects of anti-ulcer agents on these enzymes must be considered.
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PMID:Wound healing of acetic acid-induced gastric ulcer in rats and the effects of cimetidine and calcitonin, with special reference to prolylhydroxylase and collagenase enzyme activity. 764 95

Motivated by the observed influence of stainless steel and ferric and ferrous ions on the behavior of the peroxidase/oxidase oscillator, the mechanism and kinetics of interaction of 1,4-dihydronicotinamide adenine dinucleotide (NADH) with iron ions in 0.1 M acetic acid/sodium acetate buffer with pH 5.1 and with the solution/stainless steel interface were extensively studied. The character of a possible mutual influence of NADH/acetate buffer solution and Type 316 stainless steel has been investigated. We also suggest the mechanism of stainless steel corrosion inhibition by NADH. It was determined that fast complexation of ferric and ferrous ions with NADH occurred with rate constant kcompl = 4.0 x 10(9) +/- 0.2 x 10(9) M-1 s-1. The composition of the product complex is [Fe-(NADH)2] for both Fe2+ and Fe3+. A previously unreported complex of ferrous ion and NADH was discovered, determined, and separately investigated. Kinetic and equilibrium constants for reactions of iron ions-NADH complexation and following redox processes of the complex decomposition were determined from spectrophotometric and electrochemical experiments.
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PMID:Complexation of nicotinamide adenine dinucleotide with ferric and ferrous ions. 779 67


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