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:3.5.4.17 (adenosine deaminase)
5,206 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The erythrocytes of 350 pigtailed macaques (Macaca nemestrina) were examined for electrophoretic variation of hemoglobin and 26 enzymes. Seven enzymes showed variation in more than 1% of individuals: phosphoglucose isomerase, phosphoglucomutase-1, soluble NADP-dependent isocitric dehydrogenase, peptidase A, peptidase C, 2,3-diphosphoglycerate mutase, and acid phosphatase. Variation with lesser frequency was found in soluble glutamic-oxalacetic transaminase, phosphoglycerate kinase, lactic dehydrogenase, and hemoglobin. Only eight samples were tested for esterase D, and one of these had a variant phenotype. Enzymes with no clear variation were adenylate kinase, adenosine deaminase, phosphofructokinase, hexokinase, pyruvate kinase, glyceraldehyde 3-phosphate dehydrogenase, aldolase, phosphoglycerate mutase, phosphopyruvate hydratase (enolase), phosphoglucomutase-3, and superoxide dismutase. There was father-to-son transmission of PGI, PGM-1, peptidase C, 6PGD, 2,3-DPGAM, NADP-ICD, and acid phosphatase variants, suggesting that these loci are autosomal as in man.
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PMID:Intraspecific red cell enzyme variation in the pigtailed macaque (Macaca nemestrina). 114 87

Nineteen southern African isolates of Plasmodium falciparum were typed by polyacrylamide gel electrophoresis, using 5 enzymes (glucose phosphate isomerase, adenosine deaminase, lactate dehydrogenase, NADP-dependent glutamate dehydrogenase and 6-phosphogluconate dehydrogenase). Limited variation was found amongst the isolates and the frequencies of variants were similar to those of isolates from other parts of the world. Eight of the isolates contained 2 forms of glucose phosphate isomerase, indicating clonal heterogeneity. One of these 8 isolates also contained 2 forms of adenosine deaminase and another showed 2 forms of lactate dehydrogenase.
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PMID:Enzyme typing of southern African isolates of Plasmodium falciparum by polyacrylamide gel electrophoresis. 209 43

185 isolates of Plasmodium vivax were collected from patients visiting the malaria clinic run by the National Malaria Eradication Programme, Delhi, India. Percoll gradient centrifugation was used to concentrate P. vivax parasites from 0.4 to 0.5 ml of blood collected by finger prick. The parasite concentrate from each isolate was electrophoretically analysed for lactate dehydrogenase (LDH), NADP-dependent glutamate dehydrogenase (GDH), glucose phosphate isomerase (GPI) and adenosine deaminase (ADA). Variations were observed in GPI, GDH and ADA systems. Four electrophoretic forms of GPI and 5 each of GDH and ADA were observed. Electrophoretic mobilities of the different isoenzymic forms in P. vivax were identical to those reported for P. falciparum, indicating that the 2 species cannot be differentiated on the basis of electrophoretic patterns of the 4 enzyme systems studied.
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PMID:Plasmodium vivax: enzyme polymorphism in isolates of Indian origin. 269 26

A simple and fast ion pair reversed-phase high-performance liquid chromatographic method has been developed for the simultaneous determination of ATP, ADP, AMP, GTP, GDP, IMP, NADP+, NADPH+, NAD+, NADH, ADP-ribose, inosine, adenosine, hypoxanthine, and xanthine. This method allows us to have a complete picture of the most important nucleotides present in fresh human erythrocytes. Furthermore it is particularly useful in the study of the erythrocyte adenine nucleotide catabolism allowing the detection of degradation products such as IMP, inosine, adenosine, hypoxanthine, and xanthine. The separation of the compounds under investigation is achieved in less than 15 min using a reversed-phase 3-micron Supelcosil LC-18 column and adding tetrabutylammonium, as ion-pair agent, to the buffers. The short time of analysis, the high reproducibility of the system, and the accurate evaluation of the compounds of interest make this method particularly suitable for routine analysis. Finally it is possible to use this assay as an alternative method of measuring activities of enzymes which catalyze reactions involving some of these compounds, as in the case of Na+-K+ ATPase, AMP deaminase, and adenosine deaminase.
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PMID:A very fast ion-pair reversed-phase HPLC method for the separation of the most significant nucleotides and their degradation products in human red blood cells. 282 56

Homogeneous adenylate deaminase from snail foot muscle deaminated 5'-AMP, 5'-ADP, 5'-ATP and NADH with similar velocity and affinity to all substrates. At millimolar concentration NAD+ was also deaminated to a comparable extent, but NADP+, NADPH and FAD were not substrates for the snail enzyme. The amount of deaminase activity per g of fresh tissue is 5-10 times greater than in the muscle of any other species studied. The activity of the snail deaminase is regulated by pH, KCl and buffer concentrations, and Pi; however, regulation seems to be very poor in comparison with that of muscle deaminases from other species, specific to 5'-AMP. Snail enzyme appears as the first animal deaminase so far described that has such characteristics. It offers also some opportunities as an analytical tool as a consequence of its very high affinity toward adenylates.
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PMID:Direct deamination of AMP, ADP, ATP and NADH by non-specific adenylate deaminase in the foot muscle of the snail Helix pomatia. 662 80

Adenine dinucleotides such as beta-NAD, alpha-NAD, NADP, 3-aminopyridine adenine dinucleotide, flavin adenine dinucleotide, 3',5'-and 2',5'-adenylyladenosine mimicked the inhibitory effects of adenosine and adenine nucleotides on electrically evoked contractions of the rat and mouse isolated superfused vas deferens. The inhibitory effects were blocked by theophylline or adenosine deaminase, unaffected by the nucleotidase inhibitor alpha, beta-methylene ADP and enhanced by inhibition of adenosine deaminase. The inhibitory effects were associated with a release of purines from the vasa after preloading with [3H]adenosine. It is suggested that these compounds activate a receptor, causing the release of adenosine which is largely responsible for the inhibitions. Diadenosine pyrophosphate and triphosphate caused only depression of the vas twitch, whereas the pentaphosphate and hexaphosphate derivatives caused contraction, followed by inhibition at higher concentrations. These inhibitions were only partly reduced by theophylline or deaminase, but both contractile and inhibitory effects were enhanced by alpha, beta-methylene ADP. Noradrenaline contractions were also reduced by the higher polyphosphates. It is suggested that there may be a receptor for these dinucleotides, located at least in part postjunctionally. The pentaphosphate and hexaphosphate compounds mimicked the effects of nerve stimulation on the guinea-pig bladder, being substantially more potent than beta, gamma-methylene-ATP, and on the taenia caeci, where contraction or relaxation could be produced depending on resting tone.
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PMID:Actions of adenine dinucleotides on the vas deferens, guinea-pig taenia caeci and bladder. 731 4

A new spectrophotometric method for the determination of adenosine deaminase is described. Adenosine is deaminated to inosine, the latter is cleaved by an inosine-guanosine specific nucleoside phosphorylase to hypoxanthine and ribose-1-phosphate. Hypoxanthine can be oxidized further to uric acid by xanthine oxidase or to allantoin by xanthine oxidase and uricase. The hydrogen peroxide formed in these reactions is reduced by catalase to water. In the presence of high concentrations of ethanol, equivalent amounts of acetaldehyde are produced. The acetaldehyde is oxidized NAD(P) dependent and the production rate of NAD(P)H is recorded at 334 nm. The new method is suitable for the detection of adenosine deaminase in whole blood, lymphocytes, sera and tissues.
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PMID:A new spectrophotometric assay for enzymes of purine metabolism. IV. Determination of adenosine deaminase. 736 76

1. The pharmacological actions of the purine nucleotides beta-nicotinamide adenine dinucleotide (NAD), beta-nicotinamide adenine dinucleotide phosphate (beta-NADP), adenosine 5'-diphosphoribose (ADP-ribose), the vitamin nicotinamide and structural analogues of NAD and NADP were tested in the isolated perfused mesenteric arterial bed of the rat. Prejunctional effects of NAD were tested against sympathetic vasoconstriction at basal tone, and against sensory-motor vasodilatation at raised tone. 2. NAD and NADP had no vasoconstrictor action but were weak vasodilators of the raised-tone mesenteric arterial bed. A rank order of vasodilator potency of ADP >> ADP-ribose >> NADP > or = NAD = adenosine was observed. The P1-purinoceptor antagonist, 8-para-sulphophenyltheophylline (8-pST; 3 microM) inhibited vasodilator responses to NAD (pKB of 6.61 +/- 0.21, n = 7) and adenosine (pKB of 5.78 +/- 0.14, n = 6), but not those elicited by NADP, ADP and ADP-ribose. Nicotinamide, and analogues of NAD and NADP, namely nicotinamide-1,N6-ethenoadenine dinucleotide phosphate, beta-nicotinamide mononucleotide, nicotinamide hypoxanthine dinucleotide phosphate, nicotinamide hypoxanthine dinucleotide, nicotinamide guanine dinucleotide, and nicotinamide-1, N6-ethenoadenine dinucleotide had no vasoconstrictor or vasodilator actions (at doses of up to 50 nmol). 3. At basal tone, electrical field stimulation (EFS) (32 Hz, 1ms, 90 V, 5 s) at 2 min intervals elicited reproducible vasoconstrictor responses due to activation of sympathetic nerves. NAD and adenosine (10-100 microM) inhibited these responses in a concentration-dependent manner with similar potencies. Nicotinamide had no effect on sympathetic vasoconstriction at concentrations of up to 0.1 mM. Postjunctional effects of NAD (100 microM), as tested on constrictor responses to NA (5 nmol), accounted for approximately 60% inhibition at this concentration.4. In preparations in which tone had been raised with methoxamine (10-40 microM), EFS (8 Hz, 0.1ms,60 V, for 30 s) elicited vasodilatation due to activation of sensory-motor nerves. This vasodilatation was inhibited by NAD and adenosine (O.1-100 microM) in a similar concentration-dependent manner: pD2 values were 6.2 +/- 0.10 (n = 11) and 6.1 +/- 0.15 (n = 6) for NAD and adenosine respectively. Nicotinamide had no effect on sensory-motor vasodilatation at concentrations of up to 0.1 mM.5. Inhibition of sympathetic constriction by NAD and adenosine was antagonized by 8-pSPT (3 microM).Inhibitory effects of NAD and adenosine on sensory-motor vasodilatation were similarly antagonized by 8-pSPT (1 microM), pKB values were 6.72 +/- 0.21 for NAD and 6.36 +/- 0.22 for adenosine, resulting in parallel rightward shifts in the concentration-inhibitory effect curves.6. The adenosine deaminase inhibitor, pentostatin (1 microM), augmented the inhibitory effects of NAD and adenosine. Concentration-inhibitory effect curves for NAD and adenosine on sympathetic vasoconstriction and sensory-motor vasodilatation were shifted to the left without a change in the maximum.7. It is concluded that NAD can act as a modulator of sympathetic and sensory-motor transmission in rat mesenteric arteries via P1-purinoceptors possibly via direct actions but with a contribution of adenosine formed following breakdown of NAD or released pre- and/or post junctionally. Structure activity relationships of NAD, NADP, ADP and ADP-ribose showed that the P1-purinoceptor activity of NAD is abolished after removal of nicotinamide, or ribose plus nicotinamide, to yield the structurally-related ADP-ribose and ADP respectively, or when there is phosphorylation of the 2'-hydroxyl group of NAD to yield NADP.
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PMID:Modulation by nicotinamide adenine dinucleotide of sympathetic and sensory-motor neurotransmission via P1-purinoceptors in the rat mesenteric arterial bed. 759 21

Molecular abnormalities of erythroenzymopathies associated with hereditary hemolytic anemia have been determined by means of molecular biology. Pyruvate kinase (PK) deficiency is the most common and well-characterized enzyme deficiency in the glycolytic pathway, and it causes hereditary hemolytic anemia. To date, 47 gene mutations have been identified. We identified one base deletion, one splicing mutation, and six distinct missense mutations in 12 unrelated families with a homozygous PK deficiency. Mutations located near the substrate or fructose-1,6- diphosphate binding site may change the conformation of the active site, resulting in a drastic loss of activity and severe clinical symptoms. Glucose-6-phosphate dehydrogenase (G6PD)deficiency is the most common metabolic disorder, and it is associated with chronic hemolytic anemia and/or drug- or infection-induced acute hemolytic attack. An estimated 400 million people are affected worldwide. The mutations responsible for about 78 variants have been determined. Some have polymorphic frequencies in different populations. Most variants are produced by one or two nucleotide substitutions. Molecular studies have disclosed that most of the class 1 G6PD variants associated with chronic hemolysis have the mutations surrounding either the substrate or the NADP binding site. Among rare enzymopathies, missense mutations have been determined in deficiencies of glucosephosphate isomerase, (TPI), phosphoglycerate kinase, and adenylate kinase. Compound heterozygosity with missense mutation and base deletion has been determined in deficiencies of hexokinase and diphosphoglyceromutase. Compound heterozygosity with missense and nonsense mutations has been identified in TPI deficiency. One base junction mutations resulting in abnormally spliced PFK-M mRNA have been identified in homozygous PFK deficiency. An exception is hemolytic anemia due to increased adenosine deaminase activity. The basic abnormality appears to result from the overproduction of a structurally normal enzyme.
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PMID:Molecular basis of erythroenzymopathies associated with hereditary hemolytic anemia: tabulation of mutant enzymes. 857 52

The molecular abnormalities of erythroenzymopathies associated with hereditary hemolytic anemia have been determined using molecular techniques. Pyruvate kinase (PK) deficiency is the most common and well-characterized enzyme deficiency involving the glycolytic pathway and causing hereditary hemolytic anemia. We have identified six distinct missense mutations and a form of splicing mutation in 11 unrelated families with homozygous PK deficiency. Mutations located near the substrate binding site may change the conformation of the active site, resulting in a drastic loss of activity and severe clinical symptoms. Up to now, including these genetic defects, 21 missense, 1 nonsense and 2 splicing mutations, 2 insertions, and 3 deletions have been determined. G6PD deficiency is the most common metabolic disorder, and is associated with chronic and drug- or infection-induced hemolytic anemia. To date, sixty different mutations have now been identified. Except for three kinds of variants with small gene deletions or three nucleotide substitutions, all of those were found to be produced by one or two nucleotide substitutions. Molecular studies disclosed that all the class 1 variants associated with chronic hemolysis have the mutations surrounding either the substrate or the NADP binding site. Among rare enzymopathies, missense mutations have been determined in glucosephosphate isomerase deficiency, aldolase deficiency, triosephosphate isomerase (TPI) deficiency, phosphoglycerate kinase deficiency, and adenylate kinase deficiency. Compound heterozygous cases with missense mutation/nonsense mutation and missense mutation/decreased mRNA have been reported in TPI deficiency and diphosphoglyceromutase deficiency, respectively. In phosphofructokinase (PFK) deficiency, three kinds of 5'-splice junction mutations resulting in abnormally spliced PFK-M mRNA were identified. An exception is a hemolytic anemia due to increased adenosine deaminase activity. The basic abnormality appears to result from overproduction of structurally normal enzyme.
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PMID:Red cell enzymopathies as a model of inborn errors of metabolism. 862 88


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