Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: KEGG:D02003 (NBT)
 1,323 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Significant inhibition of PMN metabolic activity by F- occurred at 0.1, 0.5 and 0.0 mM F- for O2- generation, 1-C14 CO2 release labeled glucose and NBT-reduction respectively. This inhibition resulted primarily from F- suppression of nonoxidative glucose metabolism. As the concentration of F- in the O2- generating system increased beyond 10 mM, a rise in production of O2- anion occurred, peaking at 20 mM F-, followed by a rapid decline.
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PMID:Fluoride inhibition of polymorphonuclear leukocytes. 22 70

Optimal conditions for the NBT-reduction test have been sought. Increasing heparin concentrations up to 100 units per ml and a delay in performance of the test, especially when blood specimens are kept at room temperature, resulted in higher values for the NBT index, which then sometimes exceeded the upper limit of normal in healthy people and in uninfected patients. The effect of pH, composition of the buffer, and dye concentration was also investigated. Phosphate-buffered saline pH 7-2 containing 0-1% NBT dye, without glucose, gave the most reliable results. In endotoxin-stimulated NBT tests, the following procedure is recommended: incubation of 0-1 ml whole blood with lyophilised endotoxin 20 mug per ml. for 15 min. in a 37 degree C water bath, followed by the standard test with a 0-2% NBT solution. By this technique, the leucocyte reaction to various types of lipopolysaccharides was of the same order of magnitude. Drug therapy having an effect on blood components lowered this reaction, whatever the source of endotoxin used as stimulant. The importance of NBT-reduction tests is discussed. Standard conditions of test performance are strictly requisite if comparable results are to be obtained and if data not corresponding with the apparent clinical and other laboratory findings are to be evaluated correctly. The stimulated NBT test, performed in parallel with the standard test, is useful in the interpretation of abnormal results and in the detection of factors with a temporary or permanent effect on the phagocytic activity of pmn leucocytes.
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PMID:Standardisation of the nitroblue-tetrazolium test. 23 38

The effect of PHA-activated mononuclear-cell (MN) supernatants on various polymorphonuclear-leucocyte (PMN) functions were assessed. Treatment of PMN with PHA-activated MN-cell supernatants resulted in greater electrophoretic mobility, indicating an increase in the negative surface charge. PMN directional motility was inhibited in the presence of active supernatants but was not affected by a pulse exposure of the PMN to these supernatants. Neither control nor active supernatants were chemotactic for PMN, but treatment of these cells with active supernatants produced an increase in their phagocytic activity, their ability to reduce NBT and in their glucose oxidation through the hexosemonophosphate shunt. Bactericidal capacity of these PMN was unaltered. Specific loss of leucocyte inhibitory factor (LIF) activity from supernatants of PHA-activated MN cells followed their absorption with PMN cells but not with human MN cells or guinea-pig peritoneal exudate cells. Furthermore, acquired inhibition of migration of the absorbing PMN was observed.
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PMID:The effect of PHA-activated MN-cell supernatants on polymorphonuclear leucocyte function. 58 67

The effects of two chemotactic factors, endotoxin activated serm (EAS) and casein and a number of drugs known to affect intracellular cyclic nucleotide levels and various froms of neutrophil movement, on neutrophil anaerobic glycolysis and hexose monophosphate shunt (HMPS) activity were assessed. EAS caused stimulation of glycolysis. HMPS activity and NBT reduction, but casein was without effect on glycolysis and NBT reduction and inhibited HMPS activity. Drug known to increase intracellular cAMP levels caused a depression of HMPS activity whereas those reported to elevate cGMP had a variety of effects. Glycolysis was not affected by any of these agents. These results indicate a lack of relationship between cyclic nucleotide effect on cell motility and neutrophil glycolysis and HMPS activity.
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PMID:The effect of chemotactic factors and agents which influence neutrophil movement on anaerobic glycolysis and hexose monophosphate shunt activity. 68 Jul 98

Host defense mechanisms were evaluated in a 4-1/2-year-old boy with recurrent pyogenic infections and a unique hyperkeratotic skin disorder. The patient's neutrophils were consistently defective in chemotactic responsiveness but had normal NBT reduction, glucose oxidation, and iodination. Serum concentrations of IgE were markedly elevated and the secondary antibody response was abnormal. No T-cell dysfunction was detected. These findings suggest a relationship between this patient and patients with other syndromes associated with recurrent infections, cutaneous disease, defective chemotaxis, immunodeficiency, and hyperimmunoglobulinemia E.
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PMID:Defective neutrophil chemotaxis with variant ichthyosis, hyperimmunoglobulinemia E, and recurrent infections. 118 92

The original fructosamine assay, based on reduction of NBT, has been modified and marketed as a kit. The development includes addition of detergents, uricase, change of the buffer and NBT concentrations, and use of a new calibrator. We report the effects of these changes on the measured values of fructosamine in lipemic and uricemic sera. A secondary calibrator produced from pooled serum and stabilized by removal of glucose was used to calibrate the original fructosamine assay and enhance transferability of results. There was no correlation between the difference between the results obtained by the two procedures and the concentration of urate or triglycerides. The development of colour was faster with the original method. It is suggested that measurements of fructosamine by either method are practically equivalent. However, the use of polylysine as a calibrator is advantageous. It is suggested that the generic term S-Glycated proteins is used for the measurand rather than S-Fructosamine which in effect has become a commercial term.
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PMID:Influence of triglycerides and urate on methods for determination of fructosamine. 159 69

The effects of alpha- and beta-adrenergic stimulation on guinea pig eosinophil functions were studied. Both enhanced glucose uptake of eosinophils at a concentration of 5 X 10(-5) M after a 24-hour incubation. Decreased eosinophil chemotaxis and dose-dependent inhibition of arylsulfatase release from eosinophils induced by opsonized Candida albicans were observed when eosinophils were incubated with beta-adrenergic agents, but not with alpha-adrenergic agents. On the other hand, alpha stimulation inhibited phagocytosis of opsonized C. albicans by eosinophils and NBT reduction at concentrations of 8 X 10(-5) and 5 X 10(-5) M, respectively, but beta stimulation at the same concentrations did not. This suggests that the regulatory effect of adrenergic agents on phagocytosis in eosinophils is different from that in macrophages and polymorphonuclear leukocytes.
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PMID:Direct interaction of guinea pig eosinophils and adrenergic agents. 286 14

The effect of several commonly used antimalarial drugs on human peripheral blood neutrophil oxidative metabolism was studied. The following drugs were tested: chloroquine diphosphate, quinine HCl, mefloquine, proguanil HCl, cycloguanil, pyrimethamine, sulphadoxine, and tetracycline HCl. It was found that none of the antimalarial drugs examined, at clinically obtainable concentrations, had any inhibitory effect on neutrophil oxygen consumption, glucose oxidation, superoxide production, NBT reduction, and chemiluminescence. However, at higher concentrations chloroquine, quinine, mefloquine, and proguanil inhibited neutrophil oxidative burst. There was a slight enhancing effect on neutrophil oxidative metabolism by pyrimethamine, combination of pyrimethamine-sulphadoxine, cycloguanil and tetracycline at concentrations lower than the clinical levels.
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PMID:Antimalarial drugs and human neutrophil oxidative metabolism. 301 91

Insulin-glucose homeostasis was examined in 62 patients with chronic pancreatitis (CP). All patients were graded on the basis of test results from five studies: (1) endoscopic retrograde cholangiopancreatography, (2) fat-stimulated release of pancreatic polypeptide (PP), (3) NBT-bentiromide PABA test, (4) 72-hour fecal fat test, and (5) oral glucose tolerance test (OGTT). Patients with CP were graded as either mild/moderate or severe by means of a scoring system that we devised and have previously reported. Nineteen patients were graded as mild/moderate and 43 patients were graded as severe. The endocrine function of non-beta and beta islet cells was compared by assessing release of PP after fat and by release of insulin during OGTT. Release of PP was depressed in 58%, and the depressed output was found in only patients with a severe grade of CP. Forty-four of 62 patients (71%) with CP had abnormal OGTT findings; the distribution of this abnormality was not greatly different between mild/moderate and severe grades. Depressed release of insulin was seen in 58% (36 of 62)--more commonly in patients with a severe grade (10%) but also in 32% of patients with a mild/moderate grade. A subset of patients with CP sustains early beta-cell dysfunction. We conclude that decreased output of PP is a more reliable measure of functional deficit and stage in CP.
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PMID:The time course of beta cell dysfunction in chronic ethanol-induced pancreatitis: a prospective analysis. 305 70

We investigated the influence of the poly(ADP-ribose) polymerase inhibitor 3-aminobenzamide (ABA) on induction of phenotypic markers of granulocyte differentiation by retinoic acid and markers of macrophage differentiation by TPA in HL-60 cells. The differentiation of HL-60 cells towards the granulocyte lineage was assessed by hexose monophosphate shunt activity, proportion of cells capable of reducing NBT dye, and the appearance of recognizable neutrophils and bands. The effect of ABA and retinoic acid on NBT dye reduction and appearance of mature neutrophils and bands was synergistic, whereas the effects of these agents on hexose monophosphate shunt activity were additive. The differentiation inducing capacity of ABA in the presence of retinoic acid was dose-related. The influence of ABA on TPA-induced markers of macrophage differentiation was assessed by determining the proportion of adherent cells produced after treatment and by measuring acid phosphatase activity in the adherent cell fraction. In the presence of ABA, the number of cells adhering to plastic declined after day 2 of exposure to TPA, and acid phosphatase activity in adherent cells was inhibited fourfold (p = 0.01). The influence of ABA on the phenotypic markers of granulocyte and macrophage differentiation was detectable at concentrations that were not cytotoxic. The influence of ABA on HL-60 differentiation is similar to that previously reported for human bone marrow CFU-GM. Our data suggest that poly(ADP-ribose) polymerase plays a role in differentiation of HL-60 cells and that HL-60 might provide a useful model for evaluating control mechanisms involved in the differentiation of CFU-GM.
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PMID:Influence of the poly (ADP-ribose) polymerase inhibitor 3-aminobenzamide on macrophage and granulocyte differentiation of HL-60 cells. 308 78


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