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Gotowe bibliografie tematyczne / Adenosine deaminase and Metabolism / Artykuły w czasopismach

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Artykuły w czasopismach na temat „Adenosine deaminase and Metabolism”

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Data publikacji: 3 czerwca 2025

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1

Shatova, O. P., Eu V. Butenko, Eu V. Khomutov, D. S. Kaplun, I. Eu Sedakov, and I. I. Zinkovych. "Metformin impact on purine metabolism in breast cancer." Biomeditsinskaya Khimiya 62, no. 3 (2016): 302–5. http://dx.doi.org/10.18097/pbmc20166203302.

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Large-scale epidemiological and clinical studies have demonstrated the efficacy of metformin in oncology practice. However, the mechanisms of implementation of the anti-tumor effect of this drug there is still need understanding. In this study we have investigated the effect of metformin on the activity of adenosine deaminase and respectively adenosinergic immunosuppression in tumors and their microenvironment. The material of the study was taken during surgery of breast cacer patients receiveing metformin, and also patients which did not take this drug. The adenosine deaminase activity and su

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Kocic, G., J. Nikolic, T. Jevtovic-Stoimenov, et al. "L-Arginine Intake Effect on Adenine Nucleotide Metabolism in Rat Parenchymal and Reproductive Tissues." Scientific World Journal 2012 (2012): 1–4. http://dx.doi.org/10.1100/2012/208239.

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L-arginine is conditionally essetcial amino acid, required for normal cell growth, protein synthesis, ammonia detoxification, tissue growth and general performance, proposed in the treatment of men sterility and prevention of male impotence. The aim of the present paper was to estimate the activity of the enzymes of adenine nucleotide metabolism:5′-nucleotidase (5′-NU), adenosine deaminase (ADA), AMP deaminase, and xanthine oxidase (XO), during dietary intake of L-arginine for a period of four weeks of male Wistar rats. Adenosine concentration in tissues is maintained by the relative activitie

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3

Nishiyama, Akira, Shoji Kimura, Hong He, et al. "Renal interstitial adenosine metabolism during ischemia in dogs." American Journal of Physiology-Renal Physiology 280, no. 2 (2001): F231—F238. http://dx.doi.org/10.1152/ajprenal.2001.280.2.f231.

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The present study was conducted to determine the metabolism of renal interstitial adenosine under resting conditions and during ischemia. By using a microdialysis method with HPLC-fluorometric analysis, renal interstitial concentrations of adenosine, inosine, and hypoxanthine were assessed in pentobarbital-anesthetized dogs. Average basal renal interstitial concentrations of adenosine, inosine, and hypoxanthine were 0.18 ± 0.04, 0.31 ± 0.05, and 0.35 ± 0.05 μmol/l, respectively. Local inhibition of adenosine kinase with iodotubercidin (10 μmol/l in perfusate) or inhibition of adenosine deamina

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4

Schrader, W. P., and C. A. West. "Localization of adenosine deaminase and adenosine deaminase complexing protein in rabbit heart. Implications for adenosine metabolism." Circulation Research 66, no. 3 (1990): 754–62. http://dx.doi.org/10.1161/01.res.66.3.754.

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Schrader, W. P., C. A. West, and N. L. Strominger. "Localization of adenosine deaminase and adenosine deaminase complexing protein in rabbit brain." Journal of Histochemistry & Cytochemistry 35, no. 4 (1987): 443–51. http://dx.doi.org/10.1177/35.4.3546489.

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Adenosine deaminase and adenosine deaminase complexing protein have been localized in rabbit brain. Brains fixed in paraformaldehyde or in Clarke's solution were blocked coronally. Blocks from brains fixed in paraformaldehyde were either frozen in liquid nitrogen or embedded in paraffin. Tissue fixed in Clarke's solution was embedded in paraffin. Sections from each block were stained by the peroxidase-antiperoxidase method for adenosine deaminase or complexing protein using affinity-purified goat antibodies. Adenosine deaminase and complexing protein did not co-localize. Adenosine deaminase wa

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6

Ashish, Jain, Pandey* Chetan, Sharma Pandey Archana, Dutta Pritha, and Jain RJ. "Effect of 24 Hours Storage at Different Temperature on Pleural Fluid ADA (Adenosine Deaminase) Level." International Journal of Pharmacy and Biological Sciences-IJPBS 13, no. 2 (2023): 113–16. https://doi.org/10.5281/zenodo.8129772.

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Adenosine deaminase, an enzyme produced from lymphocyte and involved in purine metabolism has been extensively studied as a biochemical marker in pleural fluid during investigation for tropical pulmonary eosinophilia. The test assay, low priced, quick, barely forwarded, and can be performed in most laboratories its major physiological role is related to the proliferation and distinction of lymph cell. Pleural fluid of tuberculate start is generally lymph cell preponderant. Different cut off values of Adenosine Deaminase ranging from 30-100 IU/ L have been used in various studies with differing

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7

Schrader, W. P., C. A. West, U. H. Rudofsky, and W. A. Samsonoff. "Subcellular distribution of adenosine deaminase and adenosine deaminase-complexing protein in rabbit kidney: implications for adenosine metabolism." Journal of Histochemistry & Cytochemistry 42, no. 6 (1994): 775–82. http://dx.doi.org/10.1177/42.6.8189039.

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We evaluated the age-related distribution of adenosine deaminase (ADA) and adenosine deaminase-complexing protein (CP) in rabbit kidney by immunohistochemical staining procedures. Paraffin- or resin-embedded tissue from rabbits < 1 week-4 years of age were stained by the peroxidase-anti-peroxidase (PAP) method for ADA and CP. With the exception of neonates, the qualitative staining pattern of each protein remained generally constant with age. In the cortex, distal tubules, blood vessels, histiocytes, and epithelial cells lining Bowman's capsule stained for ADA. Proximal tubules and glomerul

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8

Dyakova, M. E., K. B. Vladimirov, D. S. Esmedlyaeva, and P. K. Yablonskiy. "Enzymes of purine metabolism — biomarkers for the diagnostics of tuberculous pleurisy in patients with HIV infection." HIV Infection and Immunosuppressive Disorders 15, no. 1 (2023): 32–40. http://dx.doi.org/10.22328/2077-9828-2023-15-1-32-40.

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The objective of the study was to evaluate the information content of determining the activity of adenosine deaminase and adenosine deaminase-2 in the diagnosis of tuberculous pleurisy in patients with HIV infection.Materials and methods. A total of 378 patients with pleural effusion were retrospectively examined. In 215 cases, tuberculous pleurisy was detected (TP); and 163 patients had non-tuberculous pleural effusion (non-TP). As much as 27 patients in the TP group were HIV co-infected (TP/HIV+), the remaining 188 patients were HIV — negative (TP/HIV–). In all the patients, the activity of

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9

Jenuth, Jack P., Ellen R. Mably, and Floyd F. Snyder. "Modelling of purine nucleoside metabolism during mouse embryonic development. Relative routes of adenosine, deoxyadenosine, and deoxyguanosine metabolism." Biochemistry and Cell Biology 74, no. 2 (1996): 219–25. http://dx.doi.org/10.1139/o96-022.

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The individual activities for adenosine kinase, deoxyadenosine kinase, adenosine deaminase, deoxyguanosine kinase, and purine nucleoside phosphorylase were determined during days 7 to 13 of mouse embryonic development. Adenosine deaminase increased 74-fold between days 7 and 9; deoxyadenosine kinase increased 5.4-fold during the same interval. Adenosine kinase, deoxyguanosine kinase, and purine nucleoside phosphorylase exhibited less than 2-fold changes in activity between days 7 and 13. Using Michaelis constants for each enzyme and the maximal velocities determined from enzyme assay, the rela

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10

Hohl, Charlene M. "AMP deaminase in piglet cardiac myocytes: effect on nucleotide metabolism during ischemia." American Journal of Physiology-Heart and Circulatory Physiology 276, no. 5 (1999): H1502—H1510. http://dx.doi.org/10.1152/ajpheart.1999.276.5.h1502.

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The purpose of this study was to examine in situ regulation of AMP deaminase in newborn piglet cardiac myocytes and to determine its role in nucleotide metabolism during ischemia. When a rapid deenergization paradigm was used to assay AMP deaminase, enzyme activity depended on the hormonal and metabolic status of cells just before deenergization. Inosine 5′-monophosphate (IMP) formation was increased 150% in deenergized myocytes pretreated with phorbol 12-myristate 13-acetate (PMA; EC50= 4.7 × 10−8M). This effect was 90% blocked with the protein kinase C (PKC) inhibitor staurosporine. In addit

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11

Dutra, Gustavo Pimentel, Gustavo L. Ottoni, Diogo R. Lara, and Maurício Reis Bogo. "Lower frequency of the low activity adenosine deaminase allelic variant (ADA1*2) in schizophrenic patients." Revista Brasileira de Psiquiatria 32, no. 3 (2010): 275–78. http://dx.doi.org/10.1590/s1516-44462010005000003.

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OBJECTIVE: Adenosine may play a role in the pathophysiology of schizophrenia, since it modulates the release of several neurotransmitters such as glutamate, dopamine, serotonin and acetylcholine, decreases neuronal activity by pos-synaptic hyperpolarization and inhibits dopaminergic activity. Adenosine deaminase participates in purine metabolism by converting adenosine into inosine. The most frequent functional polymorphism of adenosine deaminase (22G→A) (ADA1*2) exhibits 20-30% lower enzymatic activity in individuals with the G/A genotype than individuals with the G/G genotype. The aim of thi

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12

Sciotti, Veronica M., and David G. L. Van Wylen. "Increases in Interstitial Adenosine and Cerebral Blood Flow with Inhibition of Adenosine Kinase and Adenosine Deaminase." Journal of Cerebral Blood Flow & Metabolism 13, no. 2 (1993): 201–7. http://dx.doi.org/10.1038/jcbfm.1993.24.

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The purpose of this study was to determine the changes in interstitial fluid (ISF) adenosine and cerebral blood flow (CBF) during inhibition of adenosine kinase or adenosine deaminase. Brain microdialysis was used to (a) measure CBF (H2 clearance), (b) sample cerebral ISF, and (c) deliver drugs locally to the brain. Microdialysis probes were implanted bilaterally in the caudate nucleus of halothane-anesthetized rats ( n = 11). One probe was perfused with artificial cerebrospinal fluid (CSF) containing iodotubercidin (IODO), an adenosine kinase inhibitor, while the other probe was perfused with

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13

Buc, Hélène A., Laure Thuillier, Michèle Hamet, Florianne Garreau, Arlette Moncion, and Jean-Louis Pérignon. "Energy metabolism in adenosine deaminase-inhibited human erythrocytes." Clinica Chimica Acta 156, no. 1 (1986): 61–69. http://dx.doi.org/10.1016/0009-8981(86)90179-8.

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Tamaoki, J., E. Tagaya, A. Chiyotani, et al. "Effect of adenosine on adrenergic neurotransmission and modulation by endothelium in canine pulmonary artery." American Journal of Physiology-Heart and Circulatory Physiology 272, no. 3 (1997): H1100—H1105. http://dx.doi.org/10.1152/ajpheart.1997.272.3.h1100.

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To determine the effect of adenosine on adrenergic neurotransmission in pulmonary vasculature and its modulation by endothelial cells, we studied canine pulmonary arteries under isometric conditions in vitro. Adenosine decreased the contractile responses to electrical field stimulation but had no effect on those to norepinephrine. This inhibitory effect was concentration dependent, with a rank order of potency of NECA > 2-chloroadenosine > adenosine >> APNEA (an A3-adenosine-receptor agonist) > CGS-21680 (an A2a agonist) > CCPA (an A1 agonist). Adenosine reduced the electrica

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15

Szondy, Z., and E. A. Newsholme. "The rate of the AMP/adenosine substrate cycle in concanavalin-A-stimulated rat lymphocytes." Biochemical Journal 261, no. 3 (1989): 739–42. http://dx.doi.org/10.1042/bj2610739.

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The effect of adenosine on the metabolism of prelabelled adenine nucleotides was investigated in concanavalin-A-stimulated rat lymphocytes. Adenosine in the presence of the adenosine deaminase inhibitor, deoxycoformycin, caused a 2-fold increase in the ATP concentration. This effect was, in part, countereacted by an increased rate of adenine nucleotide catabolism, which could be explained by a stimulation of AMP deaminase (EC 3.5.4.6). At the same time a continuous rate of labelled adenosine production was found, which was not affected by the increased ATP concentration and which could only be

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Schimmel, R. J., L. McCarthy, and D. Dzierzanowski. "Effects of pertussis toxin treatment on metabolism in hamster brown adipocytes." American Journal of Physiology-Cell Physiology 249, no. 5 (1985): C456—C463. http://dx.doi.org/10.1152/ajpcell.1985.249.5.c456.

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This communication reports the effects of the exotoxin of Bordetella pertussis (pertussis toxin) on hamster brown fat cells. Pertussis toxin significantly increased the lipolytic and respiratory responses to isoproterenol but did not increase the basal rates of either of these processes. In contrast, the stimulation of respiration by the alpha-adrenergic agent phenylephrine was not altered by pertussis toxin. The inhibitory effects of adenosine on stimulated lipolysis, respiration, and adenylate cyclase activity were completely abolished by pertussis toxin, as was the ability of methylxanthine

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Jamal, Z., and E. D. Saggerson. "Enzymes involved in adenosine metabolism in rat white and brown adipocytes. Effects of streptozotocin-diabetes, hypothyroidism, age and sex differences." Biochemical Journal 245, no. 3 (1987): 881–86. http://dx.doi.org/10.1042/bj2450881.

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1. Adipocytes were isolated from epididymal white fat and interscapular brown fat of male rats, and activities of 5′-nucleotidase, adenosine deaminase and adenosine kinase were measured in cell extracts. 2. 5′-Nucleotidase activity in white adipocytes was increased in streptozotocin-diabetes, decreased in hypothyroidism and increased with age. That activity in brown adipocytes was unchanged in diabetes, decreased in hypothyroidism and increased with age. 5′-Nucleotidase activity was higher in white adipocytes from female rats. 3. Adenosine deaminase activity in white adipocytes was increased i

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18

Pan, Yue, Renrui Qi, Minghao Li, Bingda Wang, Honglan Huang, and Weiwei Han. "Random acceleration and steered molecular dynamics simulations reveal the (un)binding tunnels in adenosine deaminase and critical residues in tunnels." RSC Advances 10, no. 72 (2020): 43994–4002. http://dx.doi.org/10.1039/d0ra07796h.

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Aran, J. M., D. Colomer, E. Matutes, J. L. Vives-Corrons, and R. Franco. "Presence of adenosine deaminase on the surface of mononuclear blood cells: immunochemical localization using light and electron microscopy." Journal of Histochemistry & Cytochemistry 39, no. 8 (1991): 1001–8. http://dx.doi.org/10.1177/39.8.1856451.

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Adenosine deaminase, which is essential for lymphoid differentiation and function, has previously been considered to be a cytosolic enzyme. In this report we demonstrate that it can be found associated with the plasma membrane of lymphocytes. By means of immunological techniques using both light and electron microscopy, adenosine deaminase was localized on the external side of the plasma membrane of normal lymphocytes and monocytes. Since the enzyme expression differed depending on the type of cell examined, new hypotheses about the mechanisms involving purine metabolism in immune dysfunctions

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Sandhu, G. S., A. C. Burrier, and D. R. Janero. "Adenosine deaminase inhibitors attenuate ischemic injury and preserve energy balance in isolated guinea pig heart." American Journal of Physiology-Heart and Circulatory Physiology 265, no. 4 (1993): H1249—H1256. http://dx.doi.org/10.1152/ajpheart.1993.265.4.h1249.

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We investigated the effect of the adenosine deaminase inhibitors erythro-9-(2-hydroxy-3-nonyl)adenine (EHNA) and coformycin on high-energy phosphate metabolism, tissue nucleotides and nucleosides, and recovery of contractile function in isolated, perfused guinea pig hearts. EHNA and coformycin (10 microM) improved postischemic recovery of contractile function approximately 85% and enhanced coronary flow rate in reperfused tissue approximately 40%. The protective effect of EHNA on recovery of contractile function was concentration dependent. Although adenosine (10 microM) increased coronary flo

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Kutryb-Zajac, Barbara, Paulina Mierzejewska, Ewa M. Slominska, and Ryszard T. Smolenski. "Therapeutic Perspectives of Adenosine Deaminase Inhibition in Cardiovascular Diseases." Molecules 25, no. 20 (2020): 4652. http://dx.doi.org/10.3390/molecules25204652.

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Adenosine deaminase (ADA) is an enzyme of purine metabolism that irreversibly converts adenosine to inosine or 2′deoxyadenosine to 2′deoxyinosine. ADA is active both inside the cell and on the cell surface where it was found to interact with membrane proteins, such as CD26 and adenosine receptors, forming ecto-ADA (eADA). In addition to adenosine uptake, the activity of eADA is an essential mechanism that terminates adenosine signaling. This is particularly important in cardiovascular system, where adenosine protects against endothelial dysfunction, vascular inflammation, or thrombosis. Beside

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Martin, S. E., and E. L. Bockman. "Adenosine regulates blood flow and glucose uptake in adipose tissue of dogs." American Journal of Physiology-Heart and Circulatory Physiology 250, no. 6 (1986): H1127—H1135. http://dx.doi.org/10.1152/ajpheart.1986.250.6.h1127.

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Intravenous norepinephrine increases glycerol release and blood flow in adipose tissue. The vasodilation may be an indirect effect of norepinephrine through the production of adenosine. Adenosine increases glucose uptake and inhibits lipolysis in vitro. To test whether adenosine regulates blood flow and/or metabolism in vivo, adenosine deaminase (ADA) was infused intra-arterially into the inguinal fat pads of anesthetized dogs. In unstimulated tissues, ADA (n = 7) significantly increased vascular resistance and significantly decreased glucose uptake compared with the effects of a control (boil

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Holland, M. J., E. Murphy, and J. K. Kelleher. "Adenosine metabolism in human skin fibroblasts." American Journal of Physiology-Cell Physiology 248, no. 1 (1985): C21—C26. http://dx.doi.org/10.1152/ajpcell.1985.248.1.c21.

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When normal fibroblasts were incubated in media containing various initial concentrations of [8-14C]adenosine, ranging from 0.25 to 400 microM, under conditions where product formation was linear, greater than 90% of the intracellular label was found in adenine nucleotides, largely in the form of ATP, less than 1% of the intracellular label appeared in the nucleic acids, the remaining intracellular label was found in adenosine, inosine, and hypoxanthine, and the media contained two labeled products, inosine and hypoxanthine. Production of labeled inosine and hypoxanthine from adenosine was con

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Woodward, J. A., and E. D. Saggerson. "Effect of adenosine deaminase, N6-phenylisopropyladenosine and hypothyroidism on the responsiveness of rat brown adipocytes to noradrenaline." Biochemical Journal 238, no. 2 (1986): 395–403. http://dx.doi.org/10.1042/bj2380395.

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Adenosine deaminase (1 unit/ml) potentiated the lipolytic action of noradrenaline in adipocytes isolated from brown adipose tissue of 1- and 6-week-old rats by decreasing the EC50 (concn. giving 50% of maximal effect) for noradrenaline by 3-4-fold. With cells from neonatal rabbit tissue, adenosine deaminase only had a small, non-significant, effect on the EC50 for noradrenaline. Lipolysis in rat brown adipocytes was inhibited by low concentrations of N6-phenylisopropyladenosine (PIA). Rabbit cells were far less sensitive to PIA. PIA, prostaglandin E1 and nicotinate all inhibited noradrenaline-

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Dr., Suhail Ahmed Almani* Dr. Tariq Zaffar Shaikh Dr. Muhammad Iqbal Dr. Abdul Subhan Talpur Dr. Sumera Bukhari Dr. Zulfiqar Ali Qutrio Baloch. "SERUM ADENOSINE DEAMINASE LEVEL IN PATIENTS WITH TYPE 2 DIABETES MELLITUS." Indo American Journal of Pharmaceutical Sciences 04, no. 07 (2017): 1908–13. https://doi.org/10.5281/zenodo.826975.

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Objective: to evaluate the serum adenosine deaminase level in patients with type 2 diabetes mellitus at tertiary care hospital Hyderabad. Patients and Methods: This six month cross sectional descriptive study was conducted in the department of medicine at tertiary care hospital Hyderabad. The inclusion criteria of this cross sectional study (six months duration) were the individuals with uncomplicated type 2 diabetes mellitus had ≥35 years of age and both male and female gender. The study diabetic population was screened for serum adenosine deaminase level by taking 2 cc venous blood sample an

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Rounds, Sharon, Winnie Lin Yee, Doloretta D. Dawicki, Elizabeth Harrington, Nancy Parks, and Michael V. Cutaia. "Mechanism of extracellular ATP- and adenosine-induced apoptosis of cultured pulmonary artery endothelial cells." American Journal of Physiology-Lung Cellular and Molecular Physiology 275, no. 2 (1998): L379—L388. http://dx.doi.org/10.1152/ajplung.1998.275.2.l379.

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Apoptosis may be important in the exacerbation of endothelial cell injury or limitation of endothelial cell proliferation. We have found that extracellular ATP (exATP) and adenosine cause endothelial apoptosis and that the development of apoptosis is linked to intracellular metabolism of adenosine [Dawicki, D. D., D. Chatterjee, J. Wyche, and S. Rounds. Am. J. Physiol. 273 ( Lung Cell Mol. Physiol. 17): L485–L494, 1997]. In the present study, we investigated the mechanism of this effect. We found that exATP, adenosine, and the S-adenosyl-l-homocysteine (SAH) hydrolase inhibitor MDL-28842 cause

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Kislitskaya, Valentihna N., Zhandos D. Kenzhin, Berikbay Zh Kultanov, Raushan S. Dosmagambetova, and Anar A. Turmuhambetova. "Disturbance of Antioxidant Enzymes and Purine Metabolism in the Ejaculate of Men Living in Disadvantaged Areas of Kyzylorda Region." Open Access Macedonian Journal of Medical Sciences 3, no. 3 (2015): 489–92. http://dx.doi.org/10.3889/oamjms.2015.085.

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AIM: Objective of the study was to evaluate the state of the main indicators of antioxidant status and enzymes of purine metabolism in the germ cells of men living in the zone of ecological catastrophe Aral Sea region.METHODS: The criterion for inclusion is the stay of an adult in the Aral Sea area is not less than 5 years, employment in occupations with no more than 2 hazard class. Determination of the activity of adenosine deaminase (ADA) was conducted in semen by the method of Nemechek et al., 1993. Determination of the activity of catalase (CAT) was performed according by the method of Kor

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Mattig, Sabine, and Andreas Deussen. "Significance of adenosine metabolism of coronary smooth muscle cells." American Journal of Physiology-Heart and Circulatory Physiology 280, no. 1 (2001): H117—H124. http://dx.doi.org/10.1152/ajpheart.2001.280.1.h117.

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A detailed understanding of adenosine metabolism of vascular smooth muscle cells (VSMC) is highly desirable to critically evaluate possible autocrine effects of adenosine in this cell species. Therefore, this study quantified intra- and extracellular adenosine flux rates, the transmembrane concentration gradient, and the adenosine surface concentration in porcine VSMC and, for comparison, aortic endothelial cells (PAEC). Cell-covered microcarrier beads packed in a chromatography column were superfused with a HEPES buffer. With the use of specific inhibitors of adenosine kinase (iodotubericidin

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ibiş, Mehmet, Seyfettin Köklü, Fatma Meriç Yilmaz, et al. "Serum Adenosine Deaminase Levels in Pancreatic Diseases." Pancreatology 7, no. 5-6 (2007): 526–30. http://dx.doi.org/10.1159/000108970.

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Paglia, DE, WN Valentine, M. Nakatani, and RA Brockway. "AMP deaminase as a cell-age marker in transient erythroblastopenia of childhood and its role in the adenylate economy of erythrocytes." Blood 74, no. 6 (1989): 2161–65. http://dx.doi.org/10.1182/blood.v74.6.2161.2161.

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Abstract Erythrocytes from 11 patients with presumptive diagnoses of transient erythroblastopenia of childhood were evaluated retrospectively (six) or prospectively (five) for a possible relationship between erythrocyte adenosine 5′-monophosphate aminohydrolase, adenylic acid deaminase (AMP deaminase) activity and intracellular concentrations of adenine nucleotides. Older red blood cell (RBC) cohorts in these patients consistently exhibited significantly decreased activities of AMP deaminase (approximately 5% to 70% of normal control mean) in association with increased concentrations (up to th

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Paglia, DE, WN Valentine, M. Nakatani, and RA Brockway. "AMP deaminase as a cell-age marker in transient erythroblastopenia of childhood and its role in the adenylate economy of erythrocytes." Blood 74, no. 6 (1989): 2161–65. http://dx.doi.org/10.1182/blood.v74.6.2161.bloodjournal7462161.

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Erythrocytes from 11 patients with presumptive diagnoses of transient erythroblastopenia of childhood were evaluated retrospectively (six) or prospectively (five) for a possible relationship between erythrocyte adenosine 5′-monophosphate aminohydrolase, adenylic acid deaminase (AMP deaminase) activity and intracellular concentrations of adenine nucleotides. Older red blood cell (RBC) cohorts in these patients consistently exhibited significantly decreased activities of AMP deaminase (approximately 5% to 70% of normal control mean) in association with increased concentrations (up to threefold)

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Bone, Derek B. J., Doo-Sup Choi, Imogen R. Coe, and James R. Hammond. "Nucleoside/nucleobase transport and metabolism by microvascular endothelial cells isolated from ENT1−/− mice." American Journal of Physiology-Heart and Circulatory Physiology 299, no. 3 (2010): H847—H856. http://dx.doi.org/10.1152/ajpheart.00018.2010.

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Nucleoside and nucleobase uptake is integral to mammalian cell function, and its disruption has significant effects on the cardiovasculature. The predominant transporters in this regard are the equilibrative nucleoside transporter subtypes 1 (ENT1) and 2 (ENT2). To examine the role of ENT1 in more detail, we have assessed the mechanisms by which microvascular endothelial cells (MVECs) from ENT1−/− mice transport and metabolize nucleosides and nucleobases. Wild-type murine MVECs express mainly the ENT1 subtype with only trace levels of ENT2. These cells also have a Na+-independent equilibrative

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Barua, R., and MA Hossain. "Adenosine Deaminase in Diagnosis of Tuberculosis: A Review." Anwer Khan Modern Medical College Journal 5, no. 2 (2014): 43–48. http://dx.doi.org/10.3329/akmmcj.v5i2.21132.

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The diagnosis of tuberculosis (TB) continues to be a challenge in clinical practice. Traditional diagnostic methods are very useful but do not provide enough sensitivity and specificity. Adenosine deaminase (ADA) has been developed and widely used for the diagnosis of TB. ADA is an enzyme that increases in TB because of the stimulation of T-cell lymphocytes by mycobacterial antigens. This article reviews the characteristics, metabolism and clinical uses of ADA for the diagnosis of TB in clinical practices. There is sufficient data supporting yield of ADA in various body fluids for the diagnosi

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Tapbergenov, S. O., B. S. Sovetov, and A. T. Tapbergenov. "Features of influence adenosine, AMP and hyperadrenalinemiya on the immune status, metabolic enzymes of purine nucleotides and the antioxidant defense system." Biomeditsinskaya Khimiya 62, no. 6 (2016): 645–49. http://dx.doi.org/10.18097/pbmc20166206645.

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Administration of a large dose of adrenaline (4 mg/kg 60 min before analysis) increased blood levels of total leukocytes, lymphocytes, decreased T-cell suppressors, leukocyte migration inhibition reaction (LMIR) and NBT test, but increased the level of conjugated dienes (CD). Administration of AMPand adenosine increased levels of total leukocytes, lymphocytes, T- lymphocytes, T-helpers, decreased the level of malondialdehyde (MDA), LMIR, and T-cell suppressors. Sympathetic hyperactivation induced by administration of a large dose of adrenaline (4 mg/kg 60 min before analysis) was accompanied b

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Mantelli, Laura, Sandra Amerini, Fabrizio Ledda, Gianni Forti, and Mario Maggi. "The Potent Relaxant Effect of Adenosine in Rabbit Corpora Cavernosa Is Nitric Oxide Independent and Mediated by A₂ Receptors." Journal of Andrology 16, no. 4 (1995): 312–17. http://dx.doi.org/10.1002/j.1939-4640.1995.tb00535.x.

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ABSTRACT: In the present study the effect of adenosine and adenosine analogues on rabbit isolated cavernosal smooth muscle has been evaluated in comparison with the effect of acetylcholine and electrical field stimulation. In the presence of guanethidine and indomethacin, acetylcholine and electrical field stimulation relaxed the rabbit corpus cavernosum, which was precontracted with phenylephrine. The nitric oxide synthesis inhibitor, Nω‐nitro‐L‐arginine‐methylester (L‐NAME), greatly reduced the relaxation induced by electrical stimulation and completely abolished the relaxant effect of acety

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Baer, Hans P., and Richard A. Vriend. "Cytosolic enzyme leakage from isolated smooth muscle preparations." Canadian Journal of Physiology and Pharmacology 63, no. 2 (1985): 164–65. http://dx.doi.org/10.1139/y85-030.

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Several isolated smooth muscle preparations were shown to release cytosolic enzymes including adenosine deaminase, lactate dehydrogenase, and nucleoside phosphorylase under experimental conditions resembling those used in contractility or drug uptake studies. This enzyme leakage indicates significant general cell damage and suggests that experiments dealing with drug metabolism, binding, and uptake in isolated tissues must be interpreted with caution.

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Boulieu, Roselyne, Claude Bory, and Gérard Souillet. "Purine metabolism in a bone-marrow transplanted adenosine deaminase deficient patient." Clinica Chimica Acta 178, no. 3 (1988): 349–52. http://dx.doi.org/10.1016/0009-8981(88)90244-6.

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Norman, Barbara, Richard L. Sabina, and Eva Jansson. "Regulation of skeletal muscle ATP catabolism by AMPD1 genotype during sprint exercise in asymptomatic subjects." Journal of Applied Physiology 91, no. 1 (2001): 258–64. http://dx.doi.org/10.1152/jappl.2001.91.1.258.

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Deficiency of myoadenylate deaminase, the muscle isoform of AMP deaminase encoded by the AMPD1 gene, is a common myopathic condition associated with alterations in skeletal muscle energy metabolism. However, recent studies have demonstrated that most individuals harboring this genetic abnormality are asymptomatic. Therefore, 18 healthy subjects with different AMPD1 genotypes were studied during a 30-s Wingate test in order to evaluate the influence of this inherited defect in AMPD1 expression on skeletal muscle energy metabolism and exercise performance in the asymptomatic population. Exercise

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Garcia-Gil, Mercedes, Marcella Camici, Simone Allegrini, Rossana Pesi, Edoardo Petrotto, and Maria Tozzi. "Emerging Role of Purine Metabolizing Enzymes in Brain Function and Tumors." International Journal of Molecular Sciences 19, no. 11 (2018): 3598. http://dx.doi.org/10.3390/ijms19113598.

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The growing evidence of the involvement of purine compounds in signaling, of nucleotide imbalance in tumorigenesis, the discovery of purinosome and its regulation, cast new light on purine metabolism, indicating that well known biochemical pathways may still surprise. Adenosine deaminase is important not only to preserve functionality of immune system but also to ensure a correct development and function of central nervous system, probably because its activity regulates the extracellular concentration of adenosine and therefore its function in brain. A lot of work has been done on extracellula

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Spychała, J., and G. Van den Berghe. "Adenine nucleotide metabolism in isolated chicken hepatocytes." Biochemical Journal 242, no. 2 (1987): 551–58. http://dx.doi.org/10.1042/bj2420551.

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The turnover of the adenine nucleotide pool, the pathway of the degradation of AMP and the occurrence of recycling of adenosine were investigated in isolated chicken hepatocytes, in which the adenylates had been labelled by prior incubation with [14C]adenine. Under physiological conditions, 85% of the IMP synthesized by the ‘de novo’ pathway (approx. 37 nmol/min per g of cells) was catabolized directly via inosine into uric acid, and 14% was converted into adenine nucleotides. The latter were found to turn over at the rate of approx. 5 nmol/min per g of tissue. Inhibition of adenosine deaminas

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Rasheed Khan, M., S. Vinod Babu, and V. KuzhandaiVelu. "Association of serum adenosine deaminase level with atherosclerotic index in type 2 diabetes mellitus patients." Biomedicine 41, no. 1 (2021): 150–52. http://dx.doi.org/10.51248/.v41i1.551.

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Introduction and Aim:The atherosclerosis is the major cause of morbidity and mortality among diabetes population. Diabetes mellitus can accelerate atherosclerotic processes. Adenosine deaminase (ADA) plays a significant role in both glucose and lipid metabolism through adenosine. This study aimed to correlate the atherosclerotic index with adenosine deaminase levels in Type 2 diabetes mellitus patients. The aim of the study is to find the association between serum ADA levels with atherosclerotic index.  Materials and Methods: A cross sectional study conducted in 100 subjects (50 co

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Tinton, S., and P. Buc-Calderon. "Homocysteine enhances the inhibitory effect of extracellular adenosine on the synthesis of proteins in isolated rat hepatocytes." Biochemical Journal 310, no. 3 (1995): 893–96. http://dx.doi.org/10.1042/bj3100893.

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Previous work has shown that extracellular adenosine inhibits the incorporation of radiolabelled leucine into proteins in isolated rat hepatocytes [Tinton, Lefebvre, Cousin and Buc Calderon (1993) Biochim. Biophys. Acta 1176, 1-6]. In this study, we investigated whether its metabolism into adenine nucleotides, inosine or S-adenosylhomocysteine (AdoHcy) is required to induce such an impairment. Incubation of isolated hepatocytes in the presence of adenosine at 0.5 or 1 mM reduces the synthesis of proteins by about 45% after 120 min of incubation. Such an inhibition occurred without cell lysis a

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Eiymo Mwa Mpollo, Marthe-Sandrine, and Punam Malik. "Sickle Cell Disease Is Associated with Reduced Adenosine Deaminase Catalytic Activity, Resulting in Altered Adenosine Metabolism." Blood 118, no. 21 (2011): 1078. http://dx.doi.org/10.1182/blood.v118.21.1078.1078.

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Abstract Abstract 1078 Sickle cell disease (SCD), a chronic hemolytic anemia due to a mutant beta-globin, is associated with prominent inflammatory features with elevated levels of inflammation mediating molecules and an oxidative state, with elevated levels of reactive oxygen species (ROS). Additionally, elevated levels of adenosine (Ado) have recently been shown to play a role in exacerbating sickle cell pathophysiology. However, the etiology of increased Ado is unclear; and presumed to occur secondary to increased ATP release from cellular damage (Xu et al, Nature Medicine, 2010). Herein, w

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Linden, Annemie Van, and Holger K. Eltzschig. "Role of pulmonary adenosine during hypoxia: extracellular generation, signaling and metabolism by surface adenosine deaminase/CD26." Expert Opinion on Biological Therapy 7, no. 9 (2007): 1437–47. http://dx.doi.org/10.1517/14712598.7.9.1437.

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Lamontagne, R. Jason, Samantha S. Soldan, Chenhe Su, et al. "A multi-omics approach to Epstein-Barr virus immortalization of B-cells reveals EBNA1 chromatin pioneering activities targeting nucleotide metabolism." PLOS Pathogens 17, no. 1 (2021): e1009208. http://dx.doi.org/10.1371/journal.ppat.1009208.

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Epstein-Barr virus (EBV) immortalizes resting B-lymphocytes through a highly orchestrated reprogramming of host chromatin structure, transcription and metabolism. Here, we use a multi-omics-based approach to investigate these underlying mechanisms. ATAC-seq analysis of cellular chromatin showed that EBV alters over a third of accessible chromatin during the infection time course, with many of these sites overlapping transcription factors such as PU.1, Interferon Regulatory Factors (IRFs), and CTCF. Integration of RNA-seq analysis identified a complex transcriptional response and associations w

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Baroni, M. G., J. C. Alcolado, E. W. A. Needham, P. Pozzilli, J. Stocks, and D. J. Galton. "Sib-Pair Analysis of Adenosine Deaminase Locus in NIDDM." Diabetes 41, no. 12 (1992): 1640–43. http://dx.doi.org/10.2337/diab.41.12.1640.

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Baroni, M. G., J. C. Alcolado, E. W. Needham, P. Pozzilli, J. Stocks, and D. J. Galton. "Sib-pair analysis of adenosine deaminase locus in NIDDM." Diabetes 41, no. 12 (1992): 1640–43. http://dx.doi.org/10.2337/diabetes.41.12.1640.

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Greger, Janusz, and Fabianowska-Majewska Krystyna. "Different Effect Of Dgtp On 2'-Deoxyadenosine Metabolism In Mitochondria And Cytosol." Zeitschrift für Naturforschung C 47, no. 11-12 (1992): 893–97. http://dx.doi.org/10.1515/znc-1992-11-1217.

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Two enzymes participating in 2′-deoxyadenosine (dAdo) metabolism: dAdo kinase (dAdoK EC 2.7.1.76) and adenosine deaminase (ADA, EC 3.5.4.4) were partially purified from rat liver mitochondria and cytosol and influence of nucleosides and nucleotides on the activity of these enzymes were investigated. Mitochondrial and cytosol dAdoK are separate proteins, while ADA from both subcellular fractions possesses similar physical properties. dGTP, a com petitive inhibitor of mitochondrial dAdoK, inhibits cytosol ADA in a mixed way but activates mitochondrial ADA and cytosol dAdoK. A possible effect of

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Headrick, J. P., and R. J. Willis. "Adenosine formation and energy metabolism: a 31P-NMR study in isolated rat heart." American Journal of Physiology-Heart and Circulatory Physiology 258, no. 3 (1990): H617—H624. http://dx.doi.org/10.1152/ajpheart.1990.258.3.h617.

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Temporal and quantitative relations between cytosolic energy metabolism, adenosine efflux, and coronary flow were examined during 10 min of isoproterenol (ISO) infusion (60 nM) or hypoxia (5% O2) in isolated isovolumic rat heart. Myocardial metabolism was monitored using 31P-nuclear magnetic resonance spectroscopy, and venous effluent was collected and assayed for adenosine. During ISO infusion, coronary flow increased to approximately 170%, and [ATP]/[ADP] [Pi] (cytosolic phosphorylation potential) declined to less than 25% of preinfusion levels, respectively (P less than 0.001). During hypox

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Jiang, Zhuoran, Chao Wang, Zixin Wu, et al. "Enzymatic deamination of the epigenetic nucleoside N6-methyladenosine regulates gene expression." Nucleic Acids Research 49, no. 21 (2021): 12048–68. http://dx.doi.org/10.1093/nar/gkab1124.

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Abstract N6-methyladenosine (m6A) modification is the most extensively studied epigenetic modification due to its crucial role in regulating an array of biological processes. Herein, Bsu06560, formerly annotated as an adenine deaminase derived from Bacillus subtilis 168, was recognized as the first enzyme capable of metabolizing the epigenetic nucleoside N6-methyladenosine. A model of Bsu06560 was constructed, and several critical residues were putatively identified via mutational screening. Two mutants, F91L and Q150W, provided a superiorly enhanced conversion ratio of adenosine and N6-methyl

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