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)

Affinity chromatography has been used to purify adenosine deaminase from various sources: calf spleen, calf intestinal mucosa, chicken duodena and human erythrocytes. For this purpose a specific inhibitor, 9-(p-aminobenzyl) adenine, was synthesized and covalently joined to agarose. Adenosine deaminase is selectively retained by such an inhibitor-resin when highly impure solutions are chromatographed through it. After elution from the resin with guanylurea, a competitive inhibitor, the enzyme is homogeneous and can be recovered in yields of 80 percent or more and the same number of multiple forms of the enzyme is present in the purified preparation and in the crude extract.
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PMID:A general method of purification of adenosine deaminase by affinity chromatography. 112 Jun 33

To evaluate the regulation of adenine nucleotide metabolism in relation to purine enzyme activities in rat liver, human erythrocytes and cultured human skin fibroblasts, rapid and sensitive assays for the purine enzymes, adenosine deaminase (EC 2.5.4.4), adenosine kinase (EC 2.7.1.20), hyposanthine phosphoribosyltransferase (EC 2.4.28), adenine phosphoribosyltransferase (EC 2.4.2.7) and 5'-nucleotidase (EC 3.1.3.5) were standardized for these tissues. Adenosine deaminase was assayed by measuring the formation of product, inosine (plus traces of hypoxanthine), isolated chromatographically with 95% recovery of inosine. The other enzymes were assayed by isolating the labelled product or substrate nucleotides as lanthanum salts. Fibroblast enzymes were assayed using thin-layer chromatographic procedures because the high levels of 5'-nucleotidase present in this tissue interferred with the formation of LaCl3 salts. The lanthanum and the thin-layer chromatographic methods agreed within 10%. Liver cell sap had the highest activities of all purine enzymes except for 5'-nucleotidase and adenosine deaminase which were highest in fibroblasts. Erythrocytes had lowest activities of all except for hypoxanthine phosphoribosyltransferase which was intermediate between the liver and fibroblasts. Erhthrocytes were devoid of 5'-nucleotidase activity. Hepatic adenosine kinase activity was thought to control the rate of loss of adenine nucleotides in the tissue. Erythrocytes had excellent purine salvage capacity, but due to the relatively low activity of adenosine deaminase, deamination might be rate limiting in the formation of guanine nucleotides. Fibroblasts, with high levels of 5'-nucleotidase, have the potential to catabolize adenine nucleotides beyond the control od adenosine kinase. The purine salvage capacity in the three tissues was erythrocyte greater than liver greater than fibroblasts. Based on purine enzyme activities, erythrocytes offer a unique system to study adenine salvage; fibroblasts to study adenine degradation; and liver to study both salvage and degradation.
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PMID:Adenine nucleotide metabolism in relation to purine enzymes in liver, erythrocytes and cultured fibroblasts. 118 98

Report here is the isolation of adenosine deaminase deficient mutants and genetic mapping. Engineering transposon MudJ (lacZ, Kanr) was used for mutagenesis and six add:: MudJ were obtained among 20,000 Kanr transductants. Adenosine deaminase activity of these mutants were assayed and all are negative. Cotransduction analysis of add::MudJ indicated that add is 70% linked to pmi(31') and 37% linked to zxx1900::Tn10d-tet insertion which is 10% linked to purR(30'). Three points cross showed that add is located between pmi and Tn10d-tet insertion. Therefore the gene order is purR-zxx1900::Tn10d-tet-add-pmi.
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PMID:[Regulation of purine biosynthesis. I. Isolation of add:: MudJ (lacZ, Kanr) insertions and genetic mapping]. 133 59

Severe combined immunodeficiency (SCID) is a heterogeneous syndrome, due to X-linked and autosomal recessive defects. A significant proportion of the autosomal recessive forms of SCID are due to mutations at the adenosine deaminase (ADA) locus. Nine different mutations at the ADA locus, including 7 missense point mutations, have been reported in children with ADA-SCID. We could detect 5 of the 7 missense mutations associated with ADA-SCID by alterations in restriction fragments utilizing standard restriction digestion of genomic DNA and hybridization of radiolabelled ADA genomic probes to Southern transfers. We additionally developed more rapid nonradioactive methods employing digestion of genomic DNA amplified by PCR that also detected all 5 mutations. Using these methods, we have examined a sample of 45 ADA-SCID chromosomes and report that these 5 missense mutations account for one third of the ADA--chromosomes studied, with 2 mutations being relatively common.
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PMID:Five missense mutations at the adenosine deaminase locus (ADA) detected by altered restriction fragments and their frequency in ADA--patients with severe combined immunodeficiency (ADA-SCID). 134 49

Adenosine deaminase activities in sera were measured in 18 psoriatic patients, 8 mycosis fungoides patients, and 9 patients with adult T cell leukemia. Adenosine deaminase activity in the sera of the psoriatic patients showed no significant increase. An elevated adenosine deaminase activity was observed in 7 of the 8 patients with mycosis fungoides and 8 of the 9 patients with adult T cell leukemia. After chemotherapy, adenosine deaminase activity in serum of acute adult T cell leukemia was reduced. Adenosine deaminase activity in the sera of 2 patients with smoldering adult T cell leukemia was more elevated, with exacerbation of the disease. It is difficult to grade the extension of the tumors in plaque stage mycosis fungoides and smoldering adult T cell leukemia. To know the progression of the disease is critical in determining its management. These results indicate that adenosine deaminase activity in serum is one of the reliable indicators for the grading of mycosis fungoides and adult T cell leukemia.
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PMID:Adenosine deaminase activity in sera of patients with psoriasis, mycosis fungoides and adult T cell leukemia. 929 44

The role of adenosine in postprandial jejunal hyperemia was investigated by determining the effect of placement of predigested food into the jejunal lumen on blood flow and oxygen consumption before and during intra-arterial infusion of dipyridamole (1.5 microM arterial concn) or adenosine deaminase (9 U/ml arterial concn) in anesthetized dogs. Neither drug significantly altered resting jejunal blood flow and oxygen consumption. Before dipyridamole or deaminase, food placement increased blood flow by 30-36%, 26-42%, and 21-46%, and oxygen consumption by 13-22%, 21-22%, and 26-29%, during 0- to 3-, 4- to 7-, and 8- to 11-min placement periods, respectively. Adenosine deaminase abolished the entire 11-min hyperemia, whereas dipyridamole significantly enhanced the initial 7-min hyperemia (45-49%). Both drugs abolished the initial 7-min food-induced increase in oxygen consumption. Dipyridamole attenuated (14%), whereas deaminase did not alter (28%), the increased oxygen consumption that occurred at 8-11 min. Adenosine deaminase also prevented the food-induced increase in venoarterial adenosine concentration difference. In separate series of experiments, luminal placement of food significantly increased jejunal lymphatic adenosine concentration and release. Also, reactive hyperemia was accompanied by an increase in venous adenosine concentration and release. This study provides further evidence to support the thesis that adenosine plays a role in postprandial and reactive hyperemia in the canine jejunum.
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PMID:Role of adenosine in postprandial and reactive hyperemia in canine jejunum. 141 8

The role of adenosine for reactive hyperemia in normal and stunned myocardium was examined in 16 open-chest barbiturate-anesthetized pigs. Interstitial adenosine concentration was reduced or enhanced by intracoronary infusion of adenosine deaminase or the nucleoside transport inhibitor R 75231, respectively. In normal myocardium, adenosine deaminase reduced volume of hyperemia (Doppler flowmetry) after a 30-s left anterior descending coronary artery (LAD) occlusion by 20% (6-34%; P < 0.05), whereas R 75231 increased volume of hyperemia by 15% (2-24%; P < 0.05). Adenosine deaminase reduced volume of hyperemia after a 2-min LAD occlusion by 27% (13-37%; P < 0.001), whereas R 75231 increased volume of hyperemia by 66% (53-159%; P < 0.001). Adenosine deaminase and R 75231 did not affect maximal hyperemia. Volume of hyperemia after a 2-min LAD occlusion was reduced in stunned myocardium (%systolic segment length shortening reduced by approximately 45%, ultrasonic technique) but not further altered by either adenosine deaminase or R 75231. These findings show that adenosine contributes to reactive hyperemia after 30-120 s of ischemia in normal myocardium and indicate that the reduced reactive hyperemia in stunned myocardium is due to reduced accumulation of adenosine during ischemia.
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PMID:Role of adenosine for reactive hyperemia in normal and stunned porcine myocardium. 141 60

Adenosine deaminase was infused into isolated perfused guinea pig hearts to determine its effect on myocardial adenosine levels. The enzyme was administered during constant coronary flow perfusion at 6.11 +/- 0.36 ml.min-1.g-1. Venous adenosine was measured in samples of pulmonary artery effluent; epicardial and endocardial adenosine were measured with the porous nylon disk technique. Infusion of adenosine deaminase at 2.4 and 4.8 U/ml produced adenosine deaminase activity of 0.92 +/- 0.09 and 2.33 +/- 0.15 U/ml, respectively, in epicardial fluid and 1.93 +/- 0.28 and 4.84 +/- 0.47 U/ml, respectively, in endocardial fluid. Aortic pressure was unchanged by infusion of adenosine deaminase at both infusion rates. Adenosine deaminase (data from both infusion rates pooled) reduced epicardial adenosine from 0.327 +/- 0.028 to 0.139 +/- 0.022 microM, endocardial adenosine from 4.61 +/- 0.42 to 1.64 +/- 0.20 microM, and venous adenosine from 0.017 +/- 0.02 to 0.003 +/- 0.001 microM. The data indicate that infused adenosine deaminase reaches the epicardial and endocardial interstitial fluid (ISF) compartments. The absence of any effect on coronary pressure suggests that adenosine may not be involved in resting basal coronary tone. The presence of significant residual adenosine despite adenosine deaminase infusion indicates that adenosine production in the unstressed isolated guinea pig heart exceeds the degradative capacity of infused adenosine deaminase. Previous studies in which it was assumed that almost all of the endogenous adenosine is inactivated by the infusion of adenosine deaminase should be reevaluated in light of these observations.
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PMID:Effect of adenosine deaminase on cardiac interstitial adenosine. 141 80

Adenosine deaminase (ADA) was partially purified 486- and 994-fold from rat liver mitochondria and cytosol, respectively. Relative molecular mass of the enzymes from both fractions was 34,000. Km for adenosine and 2'-deoxy-adenosine were 3.08 x 10(-5) M and 3.03 x 10(-5) M for mitochondrial ADA and 3.12 x 10(-5) M and 2.87 x 10(-5) M for cytosolic ADA. The enzyme from both subcellular fractions had the maximum activity at pH 7.5-8.0, and pI 5.2 and 4.2 for mitochondrial and cytosolic enzyme, respectively. The enzyme was inhibited by erythro-9-(2-hydroxy-3-nonyl)adenine and 2'-deoxycoformycin with Ki 4.4 x 10(-7) M and 3.2 x 10(-7) M for mitochondrial ADA and 4.9 x 10(-7) M 2.8 x 10(-7) M for cytosolic ADA. Among the natural nucleoside and deoxynucleotide derivatives tested, deoxy-GTP and UTP inhibited only cytosolic adenosine deaminase by 60% and 40%, respectively.
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PMID:Adenosine deaminase: physical and chemical properties of partially purified mitochondrial and cytosol enzyme from rat liver. 144 46

Dipyridamole is proposed to increase coronary blood flow (CBF) by inhibition of adenosine uptake into cells, resulting in an increase in interstitial fluid (ISF) adenosine and an adenosine-mediated vasodilation. The purpose of this study was to determine the changes in CBF and ISF adenosine, inosine, and hypoxanthine during dipyridamole infusion in the absence or presence of adenosine receptor blockade or adenosine deaminase. To sample cardiac ISF, cardiac microdialysis probes were implanted in the left ventricular myocardium of chloralose-urethan-anesthetized dogs and perfused with Krebs-Henseleit buffer. The metabolite concentration in the effluent dialysate was used as an index of intramyocardial ISF metabolite concentration. In response to dipyridamole, CBF and dialysate adenosine concentration increased 4.4-fold and 2.2-fold, respectively, whereas dialysate inosine was unchanged and dialysate hypoxanthine decreased 50%. Adenosine receptor blockade, achieved by intracoronary 8-(p-sulfophenyl)theophylline infusion, attenuated the increase in CBF induced by dipyridamole without changing dialysate adenosine concentration. Adenosine deaminase fully attenuated the dipyridamole-induced increases in CBF and dialysate adenosine. These results demonstrate that dipyridamole increases ISF adenosine in the dog and suggest that adenosine is the sole mediator of dipyridamole-induced coronary vasodilation.
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PMID:Interstitial adenosine with dipyridamole: effect of adenosine receptor blockade and adenosine deaminase. 151 Jan 52


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