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)

Ehrlich ascites tumor cells containing radioactive ATP were incubated in vitro with a range of concentrations of 2-deoxyglucose in order to produce different rates of ATP catabolism. Concentrations of all radioactive products of ATP catabolism were measured, and apparent rates of adenylate deaminase and inosinate dehydrogenase and of adenylate and inosinate dephosphorylation were calculated. It was concluded that these processes were reggulated primarily by the rate of formation of substrate, and to a lesser extent in some cases, by substrate concentration. No evidence was obtained for regulation of these processes by the concentration of ATP. The deoxyglucose-induced catabolism of radioactive GTP was also studied. When ATP catabolism was induced by incubation with 2,4-dinitrophenol, time courses of accumulation of purine nucleoside monophosphates and rates of alternative pathways of their metabolism were quite different than when deoxyglucose was used.
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PMID:Studies of the regulation of purine nucleotide catabolism. 16 83

The in vitro destruction of tumor cells by specifically sensitized mouse lymphocytes was inhibited by adenosine; this inhibition was markedly potentiated by the presence of an inhibitor of adenosine deaminase. The inhibition of cytolysis by adenosine was accompanied by a rapid elevation in lymphocytic adenosine 3',5'-monophosphate (cyclic AMP) concentrations. Both the inhibition of cytolysis and the elevation of cyclic AMP were reversed by prolonged incubation of the lymphocytes in the presence of adenosine or, more rapidly, by removal of the adenosine. Low concentrations of adenosine also caused an elevation of cyclic AMP in human lymphocytes, and this effect of adenosine may contribute to the lack of immune response associated with adenosine deaminase deficiency.
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PMID:Adenosine inhibition of lymphocyte-mediated cytolysis: possible role of cyclic adenosine monophosphate. 16 34

Steroidogenesis by Y-1 adrenal tumor cells in culture is stimulated by ATP, adenyl-5'-yl imidodiphosphate (App(NH)), adenosine 5'(beta, alpha-methylene)triphosphate (App(CH2)p), ADP, AMP, NAD, FAD, and adenosine but not by adenine or other nucleoside triphosphates. ATP, App(NH)p, App(CH2)p, and adenosine are active in the micromolar range. Like adrenocorticotropic hormone (ACTH), the onset of stimulation is immediate and occurs to the same extent. Also active are 2'- and 5'-deoxyadenosine and 2-chloroadenosine whereas adenine xyloside, L-riboside, or arabinoside have very low activity. Stimulation is accompanied by rounding of the cells. Dipyridamole, an inhibitor of adenosine transport, increased the response to low concentrations of adenosine, suggesting that adenosine acts externally. Stimulation of steroidogenesis by adenosine or phosphorylated adenosine compounds fails to occur in the presence of crystalline adenosine deaminase, and the effect of the enzyme on adenosine, ATP, or NAD stimulation is reversed by the competitive inhibitor erythro-9-[3-(nonane-2-ol)]adenine. This suggests that the enzyme acts specifically on adenosine and a requirement for the conversion of the above compounds to adenosine seems probable. The inhibition of cAMP effects by adenosine deaminase suggests that some of its effects are also mediated by conversion to adenosine. Similar stimulation is seen in I-10 Leydig tumor cells, but an ACTH-resistant mutant of Y-1 cells, called OS-3, is relatively resistant to adenosine. Adenosine and 2-chloroadenosine stimulate adenylate cyclase in membranes from Y-1 and I-10 cells at concentrations slightly greater than are effective for steroidogenesis. Other nucleosides are ineffective. Like the NH2-terminal 24 residues of adrenocorticotropic hormone (1-24 ACTH), the adenosine effect in Y-1 membranes is rapid and is on the Vmax intercept (versus ATP) and not on the Km. In contrast to steroidogenesis, adenosine is only a partial agonist for adenylate cyclase. It effect occurs in the presence of ITP, GTP, or guanyl-5'-yl imidodiphosphate (Gpp(NH)p). Theophylline inhibits adenosine-stimulated steroidogenesis. Inhibition of adenylate cyclase occurs in the same concentration range but is of the mixed type.
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PMID:Activation of steroidogenesis and adenylate cyclase by adenosine in adrenal and Leydig tumor cells. 18 24

The search for molecular changes that may be diagnostic of malignancy in the colonic epithelium is complicated by the diversity of cell types and complex cell kinetics of a tissue in which most of the cells are destined to leave within hours or days. Methods for cell separation and nuclear fractionation now permit biochemical studies of those cells that retain or regain the capacity for DNA synthesis and that are likely to include the transformed cell population. Among the changes associated with malignant transformation to be described are alterations in nuclear protein composition and metabolism, qualitative and quantitative differences in adenosine deaminase activities, activation of the guanylate/cyclic GMP system, and modification of both DNA and chromosomal proteins by alkylating carcinogens. DNA modification to produce O6-methylguanine correlates well with the incidence of tumor induction by methylazoxymethanol. Modifications of chromosomal proteins to produce methylated derivatives of lysine and arginine have been observed after the administration of 1,2-dimethylhydrazine. Such changes are likely to lead to aberrant interactions between DNA and regulatory elements in chromatin, and may not be subject to repair.
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PMID:Overview: molecular changes associated with large bowel cancer and their potential as markers and chemotherapeutic agents. 20 Mar 43

Thymic involution of Ehrlich ascites tumor bearing Swiss and NMRI mice was associated with an increased incorporation of 3H-thymidine into thymus DNA and an enhanced activity of adenosine deaminase. The apparent depletion time constants, which were determined by the following time course of the retention of 3H-DNA, indicated that the rate cell depletion was increased in the thymus of tumor bearing mice. The results suggest that the thymic involution was correlated with an increased proliferative activity and an accelerated depletion of thymic cells.
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PMID:Cell proliferation in the thymus of Ehrlich ascites tumor bearing mice. 53 Mar 35

The metabolism of 9-beta-D-arabinofuranosyladenine (AraA) to arabinofuranosyladenine 5'-triphosphate (AraATP), an inhibitor of DNA synthesis, in mouse leukemia cells was examined by means of high-pressure liquid chromatography. AraATP was separated from naturally occurring nucleotides in acid-soluble extracts and quantitative measurements of AraATP levels were made. A potent inhibitor of adenosine deaminase (2'-deoxycoformycin; co-vidarabine), when used in combination with AraA in the treatment of leukemia-bearing mice, increased the formation of AraATP in mouse leukemia cells four- to five-fold over that obtained by treatment with AraA alone. By means of high-pressure liquid chromatography the half-life of AraATP in tumor cells could be measured. Results of such studies may be of value in planning chemotherapy regimens.
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PMID:Analysis by high-pressure liquid chromatography of 9-beta-D-arabinofuranosyladenine 5'-triphosphate levels in murine leukemia cells. 55 57

Adenosine deaminase is an important enzyme in purine metabolism, and patients with abnormal lymphocyte and erythrocyte adenosine deaminase levels have been shown to have impaired immune competence. Since immune factors have been shown to be important in patients with transitional cell carcinoma of the bladder we studied adenosine deaminase activity in the hemic cells of 48 patients with this tumor. Lymphocyte adenosine deaminase levels were elevated in patients with transitional cell carcinoma and correlated with stage, activity, clinical course and tumor resection but not with tumor grade. Erythrocyte adenosine deaminase levels also were elevated in patients with transitional cell carcinoma but did not correlate with other disease parameters. Lymphocyte adenosine deaminase activity in patients with transitional cell carcinoma may be a sensitive indicator of disease activity and further studies may provide insight into the host-tumor relationship at the enzyme level.
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PMID:Adenosine deaminase activity in patients with carcinoma of the bladder. 64 89

Drug combinations of 9-beta-D-arabinofuranosyladenine and 2'-deoxycoformycin were active in the therapy of mice with intracerebral implants of the L1210 tumor. In in vivo mouse brain adenosine deaminase studies, inhibition of 9-beta-D-arabinofuranosyladenine deamination for periods of up to 24 hr was found after a single i.p. dose of 0.002 mmole/kg.
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PMID:Therapeutic effects of 9-beta-D-arabinofuranosyladenine and 2'-deoxycoformycin combinations on intracerebral leukemia. 86 31

Erythrocyte and lymphocyte adenosine deaminase (ADA) levels were studied in 31 patients with renal cell carcinoma (RCC). Decreased lymphocyte ADA levels occurred in patients with RCC. Erythrocyte ADA levels were reduced only in blood type B and O patients. Nephrectomy resulted in a rise in lymphocyte and erythrocyte ADA levels. Progression of clinical disease was associated with a fall in lymphocyte ADA values in all patients and with a rise in erythrocyte levels only in blood type A patients. Our results suggest that changes in erythrocyte and lymphocyte ADA levels in RCC patients are acquired and may offer insight into host-tumor interactions.
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PMID:Adenosine deaminase activity in patients with renal adenocarcinoma. 89 Jun 59

The regulatory properties of adenylate deaminase (EC 3.5.4.6) from Ehrlich ascites tumor cells suggest that the reaction catalyzed by this enzyme serves to protect the cell against sharp decreases in the adenylate energy charge by removing adenosine 5'-monophosphate generated when the rate of utilization of adenosine triphosphate is suddenly increased. The enzyme is effectively inhibited under normal physiological conditions of high energy charge (0.9) and 4 to 5 mM adenine nucleotide pool size. The reaction is sharply activated by a decrease in the energy charge in the physiological range (0.9 to 0.6). At low energy charge (0.6), decrease in the size of the pool causes a marked and nonlinear decrease in the rate of the deaminase reaction. This effect presumably serves to prevent excessive depletion of the adenine nucleotide pool. Calculations based on the kinetic data obtained in this study show that the AMP deaminase reaction can account for the well-established alteration of adenine nucleotide metabolism that is observed following addition of glucose or 2-deoxyglucose to intact ascites cells.
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PMID:Role of the adenylate deaminase reaction in regulation of adenine nucleotide metabolism in Ehrlich ascites tumor cells. 94 36


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