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:3.5.4.4 (adenosine deaminase)
5,136 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Adenosine kinase, adenosine deaminase, hypoxanthine phosphoribosyltransferase, inosine-nucleoside phosphorylase, 5'-AMP deaminase and 5'-IMP nucleotidase were identified in cell-free extracts of duckling erythrocytes; no evidence for 5'-AMP nucleotidase and xanthine oxidase activity was found. The Km values for the duckling red cell enzymes were similar to those reported for human erythrocytes. Plasmodium lophurae extracts demonstrated similar enzyme activities except for 5'-AMP deaminase and 5'-IMP nucleotidase which were absent. It is proposed that during infection erythrocytic AMP is catabolized to IMP, inosine and hypoxanthine; the hypoxanthine is taken up by the plasmodium, utilized to form IMP, and this in turn is converted into adenine and guanine nucleotides.
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PMID:Purine metabolizing enzymes of Plasmodium lophurae and its host cell, the duckling (Anas domesticus) erythrocyte. 678 22

1 The effects of adenyl compounds were examined on the rat atrium and ventricle. 2 Adenosine, adenosine 5'-monophosphate, adenosine 5'-diphosphate, adenosine 5'-triphosphate (ATP) and beta, gamma-methylene ATP (APPCP) produced negative inotropic effects on the rat atrium. These inhibitory effects were antagonized by 8-phenyltheophylline (8-PT), a P1-purinoceptor antagonist, and potentiated by erythro-9-(2-hydroxy-3-nonyl) adenine (EHNA), an adenosine deaminase inhibitor, but were not affected by dipyridamole, which blocks adenosine uptake. 3 alpha, beta-Methylene ATP (APCPP), which is resistant to degradation, did not produce a similar inhibitory response in the rat atrium. 4 Adenosine did not affect the basal developed force of the rat ventricle nor did it affect the beta-adrenoceptor-mediated positive inotropic effect. 5 Very high concentrations of ATP (0.1-3 mM) produced negative inotropic effects in the rat ventricle. APPCP (0.3 mM) also produced an inhibitory response, which was significantly smaller than that produced by ATP (0.3 mM). APCPP elicited excitation rather than the expected inhibitory response. 6 The inhibitory effect of ATP in the rat ventricle was not blocked by indomethacin, 8-PT or atropine. 7 It is possible that the action of ATP in the rat ventricle is mediated via P2-purinoceptors and that the lack of inhibitory action of APCPP on the rat ventricle is due to the difference in structural conformation between ATP and APCPP. 8 It seems likely that inhibitory P1-purinoceptors are present in the rat atrium and that the inhibitory responses produced by ATP in the rat ventricle may be mediated via P2-purinoceptors.
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PMID:The effect of adenyl compounds on the rat heart. 687 43

The in vitro effects of deoxyadenosine and an adenosine deaminase inhibitor, deoxycoformycin, on the synthesis of DNA and the metabolism of purines were investigated in human leukemic T-cells. In the presence of 10 microM deoxycoformycin, the synthesis of DNA was completely inhibited by concentrations of deoxyadenosine of 10 microM or greater. In contrast, the synthesis of DNA in normal bone marrow cells was not inhibited in the presence of up to 20 microM deoxycoformycin and up to 10 microM deoxyadenosine. Following incubation of leukemia T-cells with deoxycoformycin and deoxyadenosine, there was a significant rise in the concentration of deoxyadenosine 5'-triphosphate which was accompanied by reductions in the concentrations of adenosine 5'-triphosphate and guanosine 5'-triphosphate, as revealed by high-pressure liquid chromatographic analysis. The effects of deoxycoformycin on T-cell leukemia were examined in vivo. A patient with acute T-cell leukemia in the terminal stage received five daily injections of 250 micrograms of deoxycoformycin per kg. Among the noted changes, most prominent was the drop in the leukocyte count. Initially, the cell count rose from 7,200 cells/microliters on Day 1 to 120,000 cells/microliters on Day 3. On Day 5, the cell count began to decline and reached a nadir of 600 cells/microliter on Day 10. The leukocyte count remained below 1,000 cells/microliter through Day 12. The reduction in cell count was preceded by a decline in the incorporation of [3H]thymidine in the cells, which dropped to negligible amount by Day 7. The other prominent change was a decrease in adenosine deaminase activity in both red cells and leukemic cells. Adenosine deaminase activity of red cells dropped to 5% on Day 4, and that of leukemic cells dropped to 59% on Day 5. In addition, there were considerable alterations in the concentrations of purine metabolites which were characterized by a progressive reduction in the concentrations of total purine metabolites, especially adenosine 5'-triphosphate, and a transient rise in the concentrations of deoxyadenosine 5'-triphosphate, adenosine 5'-monophosphate, and adenosine 5-diphosphate. These findings suggest that treatment with deoxycoformycin may be of therapeutic value for T-cell leukemia. It may provide opportunities for studying the purine metabolism in T-leukemic cells which could lead to better approaches to treatment.
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PMID:Effects of 2'-deoxycoformycin on the metabolism of purines and the survival of malignant cells in a patient with T-cell leukemia. 697

1. The liberation of ammonia from adenosine 5'-phosphate (AMP) and adenosine and the release of inorganic phosphate from AMP were investigated in homogenates of bovine and human parotid glands. 2. Adenosine phosphate deaminase (AMP deaminase) was purified from bovine and human parotid glands. The enzyme preparations obtained were free from adenosine deaminase and 5'-nucleotidase activities. 3. AMP incubated with human parotid gland homogenate produced inosine 5'-phosphate, adenosine, inosine and ammonia. The amount of ammonia accumulating in the incubation mixture was equal to the sum of inosine 5'-phosphate plus inosine. 4. These results demonstrate the presence in human parotid of AMP deaminase and adenosine deaminase.
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PMID:Deamination of adenosine 5'-phosphate and adenosine as a possible source of ammonia in human and bovine parotid glands. 724 42

A marked depression of evoked CA1 potentials was observed with the nucleotide analogues a,b-methylene ADP (AOPCP) and adenylimido-diphosphate (AIP) and with 2'-adenosine monophosphate (2'-AMP). While the depression elicited by 5'-nucleotides was completely antagonized by the action of adenosine deaminase, AOPCP and 2'-AMP were only partially antagonized. The findings indicate that nucleotides on their own are capable of modulating synaptic transmission but that the physiologically more prevalent 5'-AMP is mediating its effect via adenosine. By producing this membrane permeable compound and allowing its re-uptake, the 5'-nucleotidase may determine the time course of purinergic action.
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PMID:Effect of adenosine versus adenine nucleotides on evoked potentials in a rat hippocampal slice preparation. 726 30

In the isolated rat vas deferens stimulated at 0.2 Hz, [14C]labelled 5'-AMP, 5'-ADP and 5'-ATP (10 microM) inhibited twitch responses, were broken down to [14C]adenosine in the medium and incorporated into [14C]adenine ribonucleotides in the tissue. Pretreatment of tissues with 6-(2-hydroxy-5-nitrobenzyl)-thioguanosine (NBTGR), a potent inhibitor of adenosine transport, potentiated the presynaptic inhibitory action of these 5' nucleotides and reduced their incorporation in [14C]adenine nucleotides, but did not alter the appearance of [14C]adenosine in the medium. A series of 2', 3' and 5'-substituted adenine nucleotides (10 microM) inhibited the twitch responses of the vas deferens stimulated at 0.2 Hz. This effect was potentiated by NBTGR. Addition of exogenous adenosine deaminase very significantly reduced the inhibitory actions of adenosine, 5'-AMP, 5'-ADP and 5'-ATP and also reduced those of 2', 5'-ADP, NAD+ and dePCoA. The inhibitory actions of the other 2', 3' and 5' adenine nucleotides studied were not altered by exogenous adenosine deaminase. These results indicated that the presynaptic inhibitory actions of 5'-AMP, 5'-ADP and 5'-ATP in rat vas deferens predominantly result from their prior hydrolysis to adenosine whereas the 2', 3' and 5'-substituted adenine nucleotides appear to act mainly directly to inhibit transmitter release.
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PMID:Metabolism and presynaptic inhibitory activity of 2',3' and 5'-adenine nucleotides in rat vas deferens. 730 Sep 14

Hyperthyroidism induces a number of metabolic and physiological changes in the heart including hypertrophy, increase in inotropic status, and alterations of myocardial energy metabolism. The effects of hyperthyroidism on adenosine metabolism which is intimately involved in the control of many aspects of myocardial energetics, have not been clarified. The aim of this study was thus to evaluate the potential role of adenosine in the altered physiology of the hyperthyroid heart. Transport of adenosine was studied in cardiomyocytes isolated from hyperthyroid and euthyroid rats. Activities of different enzymes of purine metabolism were studied in heart homogenates and concentrations of nucleotide and creatine metabolites were determined in hearts freeze-clamped in situ. Both transport of adenosine into cardiomyocytes and the rate of intracellular phosphorylation were higher in the hyperthyroid rat. At 10 microM concentration, adenosine transport rates were 275 and 197 pmol/min/mg protein in hyperthyroid and euthyroid cardiomyocytes respectively whilst rates of adenosine phosphorylation were 250 and 180 pmol/min/mg prot. An even more pronounced difference was observed if values were expressed per number of cells due to cardiomyocyte enlargement. Hyperthyroidism was associated with a 20% increase in adenosine kinase, 30% decrease in membrane 5'-nucleotidase and 15% decrease in adenosine deaminase activities measured in heart homogenates. In addition there was a substantial depletion in the total creatine pool from 63.7 to 41.6 mumol/g dry wt, a small decrease in the adenylate pool (from 27.2 to 24.3 mumol/g dry wt) and an elevation of the guanylate pool (from 1.22 to 1.36). These results show that adenosine transport and phosphorylation capacity is enhanced in hyperthyroidism.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hyperthyroidism increases adenosine transport and metabolism in the rat heart. 759 49

The activity of adenylate deaminase, adenylate phosphatase and adenosine deaminase, as well as the endogenous content of adenine nucleotides, was examined in the heart of ageing chickens. In new-born (1-day-old) and young (20-day-old) chickens, AMP degradation in the heart seems to proceed preferentially through deamination, while in adult (1-year-old) through dephosphorylation. Compared with the adult heart, a 2-year-old one exhibits a decline of AMP catabolism. The total adenine nucleotide content and the concentration of ATP are higher in adult and aged chicken hearts, than in new-born and young ones. Adaptive mechanisms might occur in the heart of ageing chickens to ensure an adequate availability of adenine nucleotides.
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PMID:Age-related changes of AMP breakdown in chicken heart. 786 72

Previous studies showed that in cultured chick ciliary ganglion neurons and CNS glia, adenosine can be synthesized by hydrolysis of 5'-AMP and that the accumulation of the adenosine degradative products inosine and hypoxanthine was significantly greater in glial than in neuronal cultures. Furthermore, previous immunochemical and histochemical studies in brain showed that adenosine deaminase and nucleoside phosphorylase are localized in endothelial and glial cells but are absent in neurons; however, adenosine deaminase may be found in a few neurons in discrete brain regions. These results suggested that adenosine degradative pathways may be more active in glia. Thus, we have determined if there is a differential distribution of adenosine deaminase, nucleoside phosphorylase, and xanthine oxidase enzyme fluxes in glia, comparing primary cultures of central and ciliary ganglion neurons and glial cells from chick embryos. Hypoxanthine-guanine phosphoribosyltransferase and production of adenosine by S-adenosylhomocysteine hydrolase activity were also examined. Our results show that there is a distinct profile of purine metabolizing enzymes for glia and neurons in culture. Both cell types have an S-adenosylhomocysteine hydrolase, but it was more active in neurons than in glia. In contrast, in glia the enzymatic activities of xanthine oxidase (443 +/- 61 pmol/min/10(7) cells), nucleoside phosphorylase (187 +/- 8 pmol/min/10(7) cells), and adenosine deaminase (233 +/- 32 pmol/min/10(7) cells) were more active at least 100, 20, and five times, respectively, than in ciliary ganglion neurons and 100, 100, and nine times, respectively, than in central neurons.
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PMID:Differential distribution of purine metabolizing enzymes between glia and neurons. 811 1

White and brown rat adipocytes have been permeabilised by repeated exposure of the cells in suspension to high voltage electrical discharges. The resulting preparations were permeable to low molecular weight materials, e.g., cyclic AMP, propidium iodide, and were stable in suspension with little evidence of rapid resealing, or of gross damage to the cell membrane. Leakage of lactate dehydrogenase was not markedly enhanced except at voltages in excess of 2 kV cm-1 for brown adipocytes. Exogenously-added cyclic AMP stimulated lipolysis (measured as glycerol release) in the electropermeabilised adipocytes far more effectively than in intact adipocytes. In brown, but not in white, adipocytes this effect was enhanced by addition of millimolar ATP. The EC50 for stimulation of glycerol release by cyclic AMP was 0.2 microM in electropermeabilised brown adipocytes, and 2 microM and 40 microM in electropermeabilised white adipocytes obtained from weanling and adult rats respectively. The effect of cyclic AMP on lipolysis was enhanced by addition of an inhibitor of cyclic AMP phosphodiesterases and was reduced by addition of 5'-AMP, adenosine or inosine (in brown adipocytes). Addition of adenosine deaminase caused a small, but significant, enhancement of cyclic AMP-driven lipolysis. Catecholamine-driven lipolysis was observed in electropermeabilised brown and white adipocytes, especially in the presence of GTP. Adrenaline-, and to a lesser extent cyclic AMP-, driven lipolysis in electropermeabilised white adipocytes was inhibited by insulin. This effect of insulin was not enhanced by addition of GTP or of a metabolically stable GTP analogue. The results obtained establish the electropermeabilised preparation as suitable for analysis of signal transduction pathways in white and brown adipocytes.
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PMID:Studies on signal transduction mechanisms for adrenaline-driven lipolysis in white and brown adipocytes. 816 54


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