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PubMed1984

Trichosporon adeninovorans sp. nov., a yeast species utilizing adenine, xanthine, uric acid, putrescine and primary n-alkylamines as the sole source of carbon, nitrogen and energy.

A new yeast species, Trichosporon adeninovorans, was isolated from soil by the enrichment culture method. Apart from adenine, the strain utilized uric acid, guanine, xanthine, hypoxanthine, 6,8-dihydroxypurine, putrescine, propylamine, butylamine, pentylamine, hexylamine and octylamine as sole source of carbon, nitrogen and energy. The structure of the cell wall of Tr. adeninovorans was ascomycetous. On the subcellular level growth on adenine or uric acid was accompanied with the development of microbodies in the cell. These cell organelles probably were the site of urate oxidase, an enzyme that, after growth on purine substrates, together with allantoinase was present at high activities. Low activities of adenine amidohydrolase and xanthine dehydrogenase were also demonstrated.

Adenine↗
PubMed1980

Adenosine receptor activation by adenine nucleotides requires conversion of the nucleotides to adenosine.

Adenine nucleotides cause adenosine receptor-mediated increases in cyclic AMP in the VA13 human fibroblast line. Levels of adenosine accumulated in the medium are insufficient to account for the responses to adenine nucleotides. Since rapid conversion of the nucleotides to adenosine by 5'-nucleotidase in the vicinity of the receptor might account for the responses, six experimental methods were developed to distinguish between "local conversion" and direct action of the nucleotides. Results of all six methods favored local conversion. (1)5'-Nucleotidase inhibitors blocked the accumulations of cyclic AMP elicited by AMP, ADP, and ATP, but did not affect the response to adenosine. The most potent inhibitor of both conversion of AMP and response to AMP was alpha, beta-methylene-ADP (APCP). (2) Adenosine deaminase blocked the responses to AMP, ADP, ATP, and adenosine-containing coenzymes. (3) Theophylline, a specific competitive adenosine antagonist, was an insurmountable inhibitor of the increases in cyclic AMP caused by AMP, ADP, and ATP. The insurmountability was presumably due to substrate saturation of the converting enzyme 5'-nucleotidase. (4) Although ADP and ATP had partial agonist-liked dose-response curves, they did not inhibit the response to adenosine. (5) Nine cell lines which responded to adenosine were tested for response to AMP. Cell lines with high levels of 5'-nucleotidase had large responses to AMP, those with intermediate levels of 5'-nucleotidase had large or intermediate responses to AMP, and those with low 5'-nucleotidase levels did not respond to AMP. (6) Inhibition of the uptake of labelled adenosine was used as an indicator of unlabelled adenosine concentrations near the cell membrane. Unlabelled AMP inhibited uptake nearly as effectively as unlabelled adenosine. APCP reversed the inhibition by AMP but not the inhibition by adenosine. The adenosine receptor is concluded to be an entity distinct from adenine nucleotide receptors.

Adenine Nucleotides↗
PubMed1987

The relationship between the cardiac contractile function, adenine nucleotides and amino acids of cardiac tissue and mitochondria at acute respiratory hypoxia.

The effect of asphyxia and subsequent resumption of respiration on the content of adenine nucleotides and some amino acids in heart tissue and mitochondria, as well as respiration of heart mitochondria was studied in rats. The depression of cardiac contractile function during asphyxia showed a better correlation with losses in mitochondrial adenine nucleotides (ATP + ADP + AMP) than those in cardiac tissue. The decrease in the heart work index was accompanied by a decrease in state 3 respiration with glutamate and malate as well as uncoupled respiration with these substrates. This did not occur with succinate. Nonphosphorylating (state 4) respiratory rates and ADP/O ratios were slightly affected by asphyxia, when respiratory substrates of both types were used. The decreased level of glutamic acid in the tissue and mitochondria of asphyxic hearts was simultaneously observed with a significant increase of alanine in cardiac tissue and of aspartic acid in the mitochondria. The losses of intramitochondrial ATP and respiratory activity with NAD-dependent substrates during asphyxia were associated with a reduction of glutamic acid level in mitochondria. The recovery of cardiac function during resumption of respiration was related to the restoration of mitochondrial respiration supported by glutamate and malate, as well as to the restoration of mitochondrial adenine nucleotides and glutamic acid. The results suggest that the depression of cardiac function caused by acute respiratory hypoxia may be attributed to impairment of electron transport, particularly in complex I of the respiratory chain and changes in metabolism of glutamic acid.

Adenine Nucleotides↗
PubMedDate not supplied

Suppression of the degradation of adenine nucleotides during ischemia may not be a sufficient mechanism for infarct size limitation by preconditioning.

Preconditioning is known to decelerate degradation of the tissue adenine nucleotides during ischemia and to delay ischemic myocardial necrosis. However, it is not known whether these two phenomena are related. To obtain an insight into this question, the present study examined whether adenosine and B2 receptor antagonists, which block the infarct size-limiting effect of preconditioning, modify the interstitial purine levels during preconditioning and subsequent sustained ischemia. In pentobarbital anesthetized open-chest rabbits, a microdialysis probe was placed in the territory of a branch of the left coronary artery, and perfused with Ringer solution. Preconditioning was performed with 5 min ischemia/5 min reperfusion. Dialysate adenosine and inosine were elevated from the baseline values of 0.064 +/- 0.011 and 0.329 +/- 0.044 microM to 0.189 +/- 0.069 and 4.106 +/- 1.451 microM, respectively during preconditioning, but their elevation during a subsequent 20 min of ischemia was significantly lower compared with that in the non-preconditioned myocardium. This suppression of the purine accumulation during ischemia by preconditioning was not abolished by 2 micrograms/kg of Hoe 140, a specific B2 receptor antagonist, or by 10 mg/kg of 8-phenyltheophylline, a non-selective adenosine receptor antagonist. Since the doses of Hoe 140 and 8-phenyltheophylline are sufficient to block the infarct size-limiting effect of preconditioning, the present results suggest that there is a dissociation between the suppression of adenine nucleotide degradation during ischemia by preconditioning and the enhancement of myocardial resistance against infarction. Thus, it is unlikely that a reduction of adenine nucleotide utilization by preconditioning is sufficient to protect the myocardium against ischemic necrosis.

Adenine Nucleotides↗
PubMed1989

ATP formation from deoxyadenosine in human erythrocytes: evidence for a hitherto unidentified route involving adenine and S-adenosylhomocysteine hydrolase.

A novel route of ATP formation has been identified using erythrocytes from patients deficient in four different enzymes associated with ATP formation. It entails prior adenine production from deoxyadenosine (or adenosine) in a reaction involving S-adenosylhomocysteine hydrolase. The postulated route has been demonstrated in human erythrocytes which, unlike other human cells, cannot form ATP from IMP. It is based on studies by others using purified S-adenosylhomocysteine hydrolase preparations in vitro. The results provide the first confirmation that this reaction occurs in intact human cells in vitro and thus most probably in vivo. This adenine production is normally masked in intact cells by further metabolism to ATP. Clinical significance for such a route is suggested by the fact that some adenosine analogues with potent oncostatic and antiviral properties also release adenine (or analogues) in vitro.

Adenine↗
PubMed1993

N6-substituted adenine derivatives and RNA primitive catalysts.

In our search for primitive RNA catalysts, we noticed that N6-ribosyl-adenine, a compound easily synthesized under presumed prebiotic conditions, has a free imidazole group. We showed that it is, as a catalyst, a potential analogue of histidine. Furthermore, among the chemical groups involved in protein catalysis, the imidazole ring of histidine has no equivalent in the RNA world. We have synthesized aliphatic amino groups containing polymers with adenine rings linked to macromolecules by their 6-amino group. These polymers exhibit pronounced catalytic activities in the hydrolysis of p-nitrophenylacetate. We discuss here the fact that in primitive catalysis the imidazole group could have been replaced by N6-substituted adenine derivatives.

Adenine↗
PubMed1989

Origin, metabolism and function of extracellular adenine nucleotides in the blood.

In previous views the role of adenine nucleotides was thought to be confined to the intracellular space of the cell. However, research of the last decades has revealed that nucleotides also occur in the extracellular space. This survey deals with the sources, metabolism and the role in blood of the extracellular adenine mononucleotides ATP, ADP, AMP and the dinucleotides diadenosine tetraphosphate (Ap4A) and diadenosine triphosphate (Ap3A). The latter two are novel compounds, which have recently been discovered in human platelets. The mononucleotides originate from damaged tissues, from red blood cells during haemolysis, from activated platelets, the working muscle and from the nervous system, whereas the dinucleotides are exclusively released from stimulated platelets. Both the adenine mono- and the dinucleotides act as signal molecules on blood cells as well as on cells of the vascular wall, thereby modulating physiological processes such as platelet aggregation, histamine release from mast cells, regulation of vascular tone and white cell functions. In order to limit the signal effects of extracellular nucleotides, blood cells, plasma and the interior of the vessel walls are provided with nucleotide splitting enzymes: ATP, ADP and AMP are mainly degraded by ectoenzymes present on blood cells, endothelial and on smooth muscle cells, whereas dinucleotides are primarily metabolized by plasma enzymes. This review closes with the presentation of the clinical utility of Ap3A and Ap4A as tools for the diagnosis of platelet storage pool defects.

Adenine Nucleotides↗
PubMedDate not supplied

Changes of myocardial adenine nucleotide and protein synthesis during development of cardiac hypertrophy.

1. Studies on three models of cardiac hypertrophy (aortic constriction, application of isoproterenol, daily administrations of 3,3'5-triiodo-L-thyronine, respectively) reveal that the enhancement of de novo synthesis of adenine nucleotides occurs very early during the development of cardiac hypertorphy and always precedes the increase of protein synthesis. Therefore, it seems likely that the accelerated synthesis of adenine nucleotides is an important factor among those metabolic processes involved in the stimulation of protein synthesis in the hypertrophying heart. 2. As far as the mechanism for the observed enhancement of adenine nucleotide synthesis is concerned, it has been demonstrated that the available pool of 5-phosphoribosyl-l-pyrophosphate, an essential precursor substance of de novo synthesis, is increased in the hypertrophying heart due to isoproterenol and 3,3'5-triiodo-L-thyronine, respectively.

Adenine Nucleotides↗
PubMed1981

Fatty liver of growing rats fed excess lysine and its prevention by adenine or allopurinol.

Weanling male Sprague-Dawley rats were fed ad libitum 15% casein diets with and without 5.0% lysine-HCI, 0.25% adenine sulfate or 0.1% allopurinol for 2 weeks. Addition of lysine alone depressed 2-week growth from 94 to 65 g increased average daily urinary orotic acid excretion from 0.39 to 1.77 mg and increased the percentage of total liver lipids from 3.6 to 11.2. Adenine or allopurinol did not change growth but markedly enhanced lysine-induced orotic aciduria and completely prevented lysine-induced fatty livers. Reports by other show that adenine and allopurinol also prevent fatty livers or rats fed arginine-free diets or excess orotic acid. The authors conclude that lysine-induced orotic aciduria results from arginine deficiency caused by antagonism of arginine function by lysine, and that lysine-induced fatty liver probably results from a lesion identical to that produced by feeding excess orotic acid.

Adenine↗
PubMedDate not supplied

Metabolism of 9-(2-chlorobenzyl)-, 9-(2-methylbenzyl)- and 9-(2-methoxybenzyl)-adenines by hamster hepatic microsomes.

It was previously found that 9-benzyladenine (BA) was extensively N1-oxidised by animal hepatic microsomes; further, mononitrosubstitution in the phenyl moiety of BA significantly modified the N1-oxidation rates of the corresponding substrates. In order to establish whether the electronic nature or a steric effect of the substituents in the phenyl moiety is the reason for the modification of N1-oxidation rate, the metabolism of some 2'-substituted 9-benzyladenines, i.e. 9-(2-chlorobenzyl)adenine (2CBA), 9-(2-methyl-benzyl)adenine (2MBA) and 9-(2-methoxybenzyl)adenine (2MOBA), by hamster hepatic microsomes was studied. It was found that the N1-oxide was still the major metabolite for 2CBA. However, only minor amounts of N1-oxides were formed during microsomal incubation with 2MBA and 2MOBA. On the other hand, in spite of the higher N1-oxidation rate of 2CBA, its total biotransformation rate was slightly lower than the other two substrates. Like other 9-aralkyladenines previously studied, dealkylation occurred for all three substrates. It was also found that another two metabolites formed in significant amounts in the incubates from both 2MBA and 2MOBA. These metabolites were not fully characterised and their structures unknown.

Adenine↗
PubMed2003

Direct electrochemistry of DNA, guanine and adenine at a nanostructured film-modified electrode.

A nanostructured film electrode, a multi-wall carbon nanotubes (MWNT)-modified glassy carbon electrode (GCE), is described for the simultaneous determination of guanine and adenine. The properties of the MWNT-modified GCE were investigated by scanning electron microscopy (SEM) and cyclic voltammetry. The oxidation peak currents of guanine and adenine increased significantly at the MWNT-modified GCE in contrast to those at the bare GCE. The experimental parameters were optimized and a direct electrochemical method for the simultaneous determination of guanine and adenine was proposed. Using the MWNT-modified GCE, a sensitive and direct electrochemical technique for the measurement of native DNA was also developed, and the value of (G+C)/(A+T) of HCl-digested DNA was detected.

Adenine↗
PubMed1997

A method to search for similar protein local structures at ligand binding sites and its application to adenine recognition.

We have developed a method of searching for similar spatial arrangements of atoms around a given chemical moiety in proteins that bind a common ligand. The first step in this method is to consider a set of atoms that closely surround a given chemical moiety. Then, to compare the spatial arrangements of such surrounding atoms in different proteins, they are translated and rotated so that the chemical moieties are superposed on each other. Spatial arrangements of surrounding atoms in a pair of proteins are judged to be similar, when there are many corresponding atoms occupying similar spatial positions. Because the method focuses on the arrangements of surrounding atoms, it can detect structural similarities of binding sites in proteins that are dissimilar in their amino acid sequences or in their chain folds. We have applied this method to identify modes of nucleotide base recognition by proteins. An all-against-all comparison of the arrangements of atoms surrounding adenine moieties revealed an unexpected structural similarity between protein kinases, cAMP-dependent protein kinase (cAPK), and casein kinase-1 (CK1), and D-Ala:D-Ala ligase (DD-ligase) at their adenine-binding sites, despite a lack of similarity in their chain folds. The similar local structure consists of a four-residue segment and three sequentially separated residues. In particular the four-residue segments of these enzymes were found to have nearly identical conformations in their backbone parts, which are involved in the recognition of adenine. This common local structure was also found in substrate-free three-dimensional structures of other proteins that are similar to DD-ligase in the chain fold and of other protein kinases. As the proteins with different folds were found to share a common local structure, these proteins seem to constitute a remarkable example of convergent evolution for the same recognition mechanism.

Adenine↗
PubMed2000

The interactions of square platinum(II) complexes with guanine and adenine: a quantum-chemical ab initio study of metalated tautomeric forms.

The influence of binding of square planar platinum complexes on tautomeric equilibria of the DNA bases guanine and adenine was investigated using the density functional B3LYP method. Neutral trans-dichloro(amine)-, +1 charged chloro(diamine)-, and +2 charged triamine-platinum(II) species were chosen for coordination to bases. Only the N7 interaction site of the bases was considered. The calculations demonstrate that the neutral platinum adduct does not change the tautomeric equilibria of the bases. Furthermore, N7 binding of the neutral Pt adduct moderately reduces the probability of protonation of the N1 position of adenine. Larger effects can be observed for +1 and mainly +2 adducts, but these can be rationalized by electrostatic effects. Since the electrostatic effects are expected to be efficiently compensated for by a charged backbone of DNA and counterions in a polar solvent, no dramatic increase in mispair formation is predicted for Pt(II) adducts, which is in agreement with experiment. The interaction energies between Pt adducts and the nucleobases were also evaluated. These interaction energies range from ca. 210 kJ/mol for neutral adducts, interacting with both bases and their tautomers, up to 500 kJ/mol for the +2 charged adducts, interacting with the keto-guanine tautomer and the anti-imino-adenine tautomer. The surprisingly large interaction energy for the latter structure is due to the strong H-bond between the NH3 ligand group of the metal adduct and the N6 nitrogen atom of the base.

Adenine↗
PubMed1999

Metal ions in non-complementary DNA base pairs: an ab initio study of Cu(I), Ag(I), and Au(I) complexes with the cytosine-adenine base pair.

Ab initio calculations have been carried out to characterize the structure and energetics of a silver(I) complex with the cytosine-adenine DNA base pair and an aqua ligand in the coordination sphere of Ag. In addition, we have also studied analogous complexes with Cu(I) and Au(I), and structures in which adenine has been replaced by purine in order to investigate the structural role of the adenine amino group. The calculations revealed that all metal-modified structures are dominated by the metal-base interactions, while the water-metal ion interaction and many-body interligand repulsion are less important contributions. Nevertheless, the structural role of the water molecule in the complex is quite apparent and in agreement with an earlier crystallographic study. The metal-modified base pairs exhibit large conformational flexibility toward out-of-plane motions (propeller twist and buckle), comparable or, in some cases, even larger than that observed in the base pairs without metal ions. All structures have been optimized within the Hartree-Fock approximation, while interaction energies were evaluated with the inclusion of electron correlation.

Adenine↗
PubMed2005

Gene replacement of adenylate kinase in the gram-positive thermophile Geobacillus stearothermophilus disrupts adenine nucleotide homeostasis and reduces cell viability.

Thermophilic bacteria are of great value for industry and research communities. Unfortunately, the cellular processes and mechanisms of these organisms remain largely understudied. In the present study, we investigate how the inactivation of adenylate kinase (AK) affects the adenine nucleotide homeostasis of a gram-positive moderate thermophile, Geobacillus stearothermophilus strain NUB3621-R. AK plays a major role in the adenine nucleotide homeostasis of living cells and has been shown to be essential for the gram-negative mesophile Escherichia coli. To study the role of AK in the maintenance of adenylate energy charge (EC) and cell viability of G. stearothermophilus, we generated a recombinant strain of this organism in which its endogenous gene coding for the essential protein adenylate kinase (AK) has been replaced with the adk gene from the mesophile Bacillus subtilis. PCR, DNA sequencing and Southern analysis were performed to confirm proper gene replacement and preservation of neighboring genes. The highest growing temperature for recombinant cells was almost 20 degrees C lower than for wild-type cells (56 vs. 75 degrees C). This temperature-sensitive phenotype was secondary to heat inactivation of B. subtilis AK, as evidenced by enzyme activity assays and EC measurements. At higher temperatures (65 degrees C), recombinant cells also had lower EC values (0.09) compared to wild-type cells (0.45), which reflects a disruption of adenine nucleotide homeostasis following AK inactivation.

Adenine Nucleotides↗
PubMed1992

Myocardial adenine nucleotide concentrations and myocardial norepinephrine content in patients with heart failure secondary to idiopathic dilated or ischemic cardiomyopathy.

It has been suggested that chronically reduced myocardial adenosine triphosphate (ATP) content causes contractile dysfunction in dilated cardiomyopathy. Because total adenine nucleotides (ATP, adenosine diphosphate and monophosphate) may reflect chronic changes in energy metabolism better than may ATP alone, myocardial ATP, and adenosine diphosphate and monophosphate were determined in endomyocardial biopsy specimens from 19 patients with dilated cardiomyopathy, and decreased left (30 +/- 2%) and right (34 +/- 3%) ventricular ejection fractions, and from 11 patients with ischemic cardiomyopathy (left ventricular ejection fraction 38 +/- 3%), and compared with those from 28 normal control subjects (ejection fraction greater than 55%) to assess myocardial energy metabolism in heart failure. Myocardial norepinephrine was measured simultaneously in the same biopsy specimens to assess if the myocardium studied for adenine nucleotide content was metabolically altered. Myocardial total adenine nucleotides as well as ATP levels in 19 patients with dilated cardiomyopathy (39 +/- 3 and 23 +/- 3 nmol/mg of noncollagen protein, respectively) were unchanged in comparison with those of control subjects (37 +/- 4 and 23 +/- 3, respectively); patients with ischemic cardiomyopathy were not significantly different (30 +/- 3 and 19 +/- 3, respectively). Myocardial norepinephrine in the same biopsy specimens from patients with dilated (5.8 +/- 1.1 pg/micrograms of noncollagen protein) or ischemic (5.7 +/- 1.3) cardiomyopathy was significantly decreased compared with that of normal control subjects (12 +/- 1.1).(ABSTRACT TRUNCATED AT 250 WORDS)

Adenine Nucleotides↗
PubMed1975

Intravenous adenine arabinoside against herpes simplex keratouveitis in humans.

Adenine arabinoside possessed all of the desirable characteristics for an antiviral agent: (1) not incorporated into host DNA; (2) broad spectrum activity against the DNA family of viruses; (3) lack of resistance in vitro; (4) rapid excretion; (5) did not cause immunosuppression; (6) low toxicity in significantly effective doses; and (m7) relatively inexpensive. Adenine arabinoside employed in 20 mg/kg1day intravenous infusions for seven days in a controlled series of patients was clearly effective in treating herpetic keratouveitis with only minimal adverse reactions. For the first time there may be an effective specific treatment for herpetic stromal disease and iritis. Further controlled studies comparing the effectiveness of adenine arabinoside with and without concommitant topical corticosteroid therapy are necessary.

Adenine↗
PubMed1993

Preimplantation alteration of adenine nucleotides in cryopreserved heart valves.

To assess the initial metabolic phase of cellular injury from cardiac valve processing, high-energy phosphate concentrations were analyzed in valve leaflets subsequent to critical processing steps. Using a porcine model, valves were processed in a manner identical to human homografts, with 58 randomly assigned to five groups representing distinct preparation phases. Group I (controls) sustained 40 minutes of warm ischemia concluded by liquid nitrogen immersion. Remaining groups similarly endured 40 minutes of ischemia, but were subsequently prepared according to stepwise design: II, warm ischemia + 24 hours of 4 degrees C ischemia; III, warm ischemia + 24 hours of 4 degrees C antibiotic disinfection; IV, warm ischemia + 24 hours at 4 degrees C (without antibiotics) + cryopreservation (-1 degrees C/min cryoprotected freezing); and V, warm ischemia+disinfection+cryopreservation. At each regimen's conclusion leaflet extracts were assayed by high-performance liquid chromatography for high-energy adenine nucleotides (adenosine triphosphate, adenosine diphosphate, adenosine monophosphate) and catabolites. A 47% and 86% decrease in cellular adenosine triphosphate level was observed in group III and group V leaflets, respectively. The level of total adenine nucleotides was maintained up to cryopreservation; thereafter a 74% decrease was noted. Catabolite analysis confirmed incomplete degradation of adenine nucleotides indicating cellular metabolic resilience throughout standard homograft preparation in valves previously exposed to 40 minutes of warm ischemia.

Adenine Nucleotides↗