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)

A prospective study of 111 adult patients with a pleural effusion was carried out in an area with a high prevalence of tuberculosis to compare the yield of bedside with laboratory inoculation of pleural fluid, and the yield and speed of a radiometric mycobacterial culture system (BACTEC) with that of conventional culture. The use of adenosine deaminase activity in pleural fluid as a diagnostic test for tuberculosis was also evaluated. In the 62 cases of tuberculosis confirmed histologically or by culture, or both, the BACTEC system had the same culture yield as conventional mycobacterial culture (positive in 14 cases-23%), but was significantly faster (18 versus 33 days). Bedside inoculation had a culture yield significantly higher than laboratory inoculation in the 24 patients tested (11 versus four). The remaining three diagnostic categories were malignant (28), miscellaneous (10), and undiagnosed (11). Median adenosine deaminase activity was significantly higher in tuberculous effusions than in any of the other categories, but there was considerable overlap between the groups. It is concluded that the BACTEC system is significantly faster than conventional mycobacterial culture and that bedside inoculation of pleural fluid substantially increases culture yield. Adenosine deaminase does not provide as valuable a diagnostic test of pleural tuberculosis as has been suggested.
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PMID:Tuberculous pleural effusions: increased culture yield with bedside inoculation of pleural fluid and poor diagnostic value of adenosine deaminase. 190 72

A 53-year-old woman was admitted to our hospital due to high fever, arthralgia and skin rash. Main laboratory data included the following: WBC 17,100/mm, GOT 58 U, GPT 47 U, LDH 1,510 U, ferritin 19,000 ng/ml, adenosine deaminase 79.1 U/l. She was diagnosed as having adult-onset Still's disease. Aspirin (3.0 g/day) and prednisolone (40 mg/day) were administered. All the symptoms and laboratory data improved rapidly. Adenosine deaminase, ferritin, and LDH are considered to originate mainly from the liver. Liver injury in this disease may be a primary lesion, and various serum markers may be associated with the liver abnormalities.
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PMID:Adult-onset Still's disease: hepatic involvement and various serum markers relating to the disease activity. 192 Sep 66

1. Insulin increased basal 2-deoxyglucose uptake in isolated swine adipocytes by 75%. In the absence of insulin, isoproterenol did not inhibit basal 2-deoxyglucose transport. 2. Adenosine deaminase plus isoproterenol or theophylline alone reduced insulin effect by 10 and 40%, respectively. Isoproterenol alone or with 2-chloroadenosine did not inhibit insulin effect on glucose transport activity. 3. Insulin effect was inhibited by isoproterenol in the presence of theophylline but not in the presence of adenosine deaminase. 4. These results suggest that catecholamines do not counter-regulate basal and insulin-stimulated glucose transport in swine adipocytes.
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PMID:Effect of insulin and adrenergic agonists on glucose transport of porcine adipocytes. 198 40

8-Chloroadenosine 3',5'-monophosphate has been reported to inhibit growth of various mammalian cell lines at micromolar concentrations. We have used Chinese hamster ovary cell lines with mutated cyclic AMP-dependent protein kinase or altered cyclic nucleotide metabolism to show that a metabolite, 8-chloroadenosine, is formed in the medium and is the active inhibitor of cell growth in Chinese hamster ovary cells. Adding adenosine deaminase to the Chinese hamster ovary cell growth media removes the inhibition of cell growth attributed to 8-chloroadenosine 3',5'-monophosphate. Adenosine deaminase or dipyridamole also protects Molt-4 lymphoblasts from the growth-inhibitory effects of 8-chloroadenosine 3',5'-monophosphate.
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PMID:8-Chloroadenosine 3',5'-monophosphate inhibits the growth of Chinese hamster ovary and Molt-4 cells through its adenosine metabolite. 193 80

Adenosine deaminase (ADA) activity was studied in serum and peripheral blood lymphocytes of leprosy patients and healthy controls. Serum ADA levels were found to be elevated in tuberculoid as well as lepromatous cases compared to control subjects. Serum ADA activity was significantly higher in tuberculoid cases than in the lepromatous group. Lymphocyte adenosine deaminase activity showed a similar trend. These results suggest that, since the overall activity of the enzyme is not deficient in leprosy, the cellular immune abberation seen in the different types of leprosy may be due to abnormal proliferation of different subsets of lymphocytes in response to M. leprae.
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PMID:Adenosine deaminase activity in leprosy. 208 83

Media supplemented with purine (7H-imidazo[4,5-d]pyrimidine) or the purine analogue 2,6-diaminopurine (DAP) can be employed to select several classes of purine-resistant variants from mutagenized cultures of Drosophila. One class results in elevated resistance to purine and diaminopurine which is correlated with elevated activity of the enzyme adenosine deaminase (adenosine aminohydrolase = EC 3.5.4.4). The first member of this class, Pur R, maps to position 82 +/- in the right arm of the second chromosome. The Pur R mutation causes an elevation of adenosine deaminase (ADA) enzyme activity, apparently by altering a thermolabile, ADA-specific repressor. Pur R may thus encode a negative regulator of adenosine deaminase activity similar to the ADA-binding protein found in mammalian systems.
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PMID:The PurR mutation of Drosophila melanogaster confers resistance to purine and 2,6-diaminopurine by elevating adenosine deaminase activity. 210 78

The hyperfiltration action of atrial natriuretic factor (ANF) and glucagon is accompanied by an elevation of adenosine in urine. We employed adenosine deaminase to evaluate the role of intrarenal adenosine in glomerular hyperfiltration induced by those hormones. Administration of ANF (2 micrograms/kg/min) resulted in an increase in the glomerular filtration rate (GFR): 1.99 vs. 3.01 ml/min (p less than 0.02) which was associated with a rise of adenosine excretion 87 vs. 151 pmol/min. Similarly, infusion of glucagon (2 micrograms/kg/min) raised the GFR from 1.86 to 2.67 ml/min (p less than 0.02) and adenosine excretion from 105 to 178 pmol/min (p less than 0.02). Adenosine deaminase treatment (2 U x kg/min) did not change the basal GFR and renal plasma flow but decreased plasma adenosine level 0.64 vs. 0.18 microM (p less than 0.001) and its excretion: 93 vs. 13 pmol/min (p less than 0.01). In adenosine deaminase treated rats ANF dramatically increased the GFR from 2.09 to 4.18 ml/min (p less than 0.001) and fractional filtration from 0.29 to 0.57, and the increase persisted throughout infusion of ANF. Similarly, adenosine deaminase treatment potentiated and prolonged the effect of glucagon on the GFR. These data indicate that depletion in renal adenosine does not decrease the GFR and that adenosine is present at inhibitory concentrations only during hormonal stimulation of glomerular filtration. It is concluded that renal endogenous adenosine functions do restrain hyperfiltration induced by ANF or glucagon.
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PMID:Intrarenal adenosine prevents hyperfiltration induced by atrial natriuretic factor. 213 65

Age-related changes in the activity of thymidine- and adenosine-metabolizing enzymes were studied in healthy females and those with breast cancer aged 46-70 years. A significant increase in activity of thymidine kinase, adenosine deaminase and 5'-nucleotidase and a decrease in that of thymidine phosphorylase were registered in blood serum of breast cancer patients of all age brackets. Adenosine deaminase activity in blood serum and lymphocytes of breast cancer patients was found to significantly change after surgery. A direct correlation was established between pretreatment thymidine phosphorylase activity and histological type of tumor, on the one hand and results of chemotherapy, on the other. The applicability of enzyme level assay for evaluating response to pre- and postoperative medication was studied.
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PMID:[Activity of the enzymes of DNA metabolism in the blood of patients with breast cancer]. 215 96

We have previously characterized mutant adenosine deaminase (ADA; adenosine aminohydrolase, EC 3.5.4.4) enzymes in seven children with partial ADA deficiency. Six children shared common origins, suggesting a common progenitor. However, we found evidence for multiple phenotypically different mutant enzymes. We hypothesized that many of the mutations would be at CpG dinucleotides, hot spots at which spontaneous deamination of 5-methylcytosine results in C to T or G to A transitions. Digestion of DNA from these children with Msp I and Taq I, enzymes recognizing CpG dinucleotides, identified three different mutations, each correlating with expression of a different mutant enzyme. Sequencing of cDNA clones and genomic DNA amplified by polymerase chain reaction confirmed the presence of C to T or G to A transitions at CpG dinucleotides (C226 to T, G446 to A, and C821 to T, resulting in Arg76 to Trp, Arg149 to Gln, and Pro274 to Leu). A "null" mutation, also found in two ADA-deficient severe combined immunodeficient children, was serendipitously detected as gain of a site for Msp I. Simultaneous loss of a site for Bal I defined the precise base substitution (T320 to C, Leu107 to Pro), confirmed by sequence analysis. To determine the true frequency of hot spot mutation in these children, consecutively ascertained through a newborn screening program, we sequenced cDNA from the remaining alleles. Two others were hot spot mutations (C631 to T and G643 to A, resulting in Arg211 to Cys and Ala215 to Thr), each again resulting in expression of a phenotypically different mutant enzyme. Only one additional mutation (previously identified by us) is not in a hot spot. These seven mutations account for all 14 chromosomes in these children. There is thus a very high frequency of hot spot mutations in partial ADA deficiency. Most of these children carry two different mutant alleles. We were able to correlate genotype and phenotype and to dissect the activity of individual mutant alleles.
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PMID:Hot spot mutations in adenosine deaminase deficiency. 216 47

This study examined the precision of central fiber growth in a subpopulation of dorsal root ganglion neurons in developing mouse spinal cord. Immunohistochemical techniques using a monospecific, polyclonal antiserum to mouse adenosine deaminase (ADA) were utilized to label a population of primary sensory afferents that have been found to exclusively innervate laminae I and II of the dorsal horn in adult mice. Initial growth of ADA-immunoreactive (ADA-IR) primary afferents occurred very early in development, embryonic day 10 (E10), a time coincident with the earliest settling time of dorsal root ganglion neurons. Adenosine deaminase immunoreactive primary afferents were observed throughout the cross-sectional area of the primordial dorsal funiculus (DF) as early as E10. Immunostained fibers remained quiescent in the DF during its growth and separation into the tract of Lissauer and dorsal column pathway. By E15, the two pathways had formed and ADA-IR fibers were observed exclusively in the tract of Lissauer. This segregation of fibers remained throughout development and reflected the adult pattern. Growth was reinitiated at E16 when the fibers advanced into the dorsal horn and proceeded directly to laminae I and II mimicking their adult distribution. Exuberant fiber growth was not detected throughout their development. These results strongly suggest that ADA-IR fibers exhibit precise fiber guidance to a preferred pathway, the tract of Lissauer, and accurate laminar innervation of the dorsal horn.
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PMID:Axonal guidance of adenosine deaminase immunoreactive primary afferent fibers in developing mouse spinal cord. 222 41


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