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PubMed1990

Regulation of photolyase in Escherichia coli K-12 during adenine deprivation.

DNA photolyase, a DNA repair enzyme encoded by the phr gene of Escherichia coli, is normally regulated at 10 to 20 active molecules per cell. In purA mutants deprived of adenine, this amount increased sixfold within 2 h. Operon fusions placing lacZ under transcriptional control of phr promoters indicated no change in transcription rate during adenine deprivation, and gene fusions of phr with lacZ showed a nearly constant level of translation as well. Immunoblot analysis indicated that the total amount of photolyase protein remained constant during enzyme amplification. On the other hand, treatment of cells with chloramphenicol during the adenine deprivation prevented any increase. DNA regions lying 1.3 to 4.2 kb upstream of the phr coding sequences were necessary for this amplification to occur and for this purpose would function in trans. These results suggest that adenine deprivation leads to a posttranslational change, involving synthesis of protein encoded by sequences lying upstream of phr, which increases photolyase activity. The amplification in activity was found to be reversible, for when adenine was restored, the photolyase activity declined before cell growth resumed.

Adenine↗
PubMed1977

Fructose-induced adenine nucleotide catabolism in isolated rat hepatocytes.

The mechanism of fructose-induced nucleotide catabolism was studied using isolated rat hepatocytes in which the adenine nucleotide pool was prelabelled with [14C]adenine. Incubation of these cells with fructose caused a rapid depletion of the adenine nucleotides and a corresponding increase in allantoin. There was no accumulation of radioactivity in adenosine in the presence or absence of the adenosine deaminase inhibitor 9-erythro-(2-hydroxy-3-nonyl)adenine. This confirms the previous hypothesis that fructose-induced adenine nucleotide catabolism occurs by way of AMP deaminase (AMP amino-hydrolase, EC 3.5.4.6).

AMP Deaminase↗
PubMed1988

De novo synthesis of adenine nucleotides in different skeletal muscle fiber types.

Management of adenine nucleotide catabolism differs among skeletal muscle fiber types. This study evaluated whether there are corresponding differences in the rates of de novo synthesis of adenine nucleotide among fiber type sections of skeletal muscle using an isolated perfused rat hindquarter preparation. Label incorporation into adenine nucleotides from the [1-14C]glycine precursor was determined and used to calculate synthesis rates based on the intracellular glycine specific radioactivity. Results show that intracellular glycine is closely related to the direct precursor pool. Rates of de novo synthesis were highest in fast-twitch red muscle (57.0 +/- 4.0, 58.2 +/- 4.4 nmol.h-1.g-1; deep red gastrocnemius and vastus lateralis), relatively high in slow-twitch red muscle (47.0 +/- 3.1; soleus), and low in fast-twitch white muscle (26.1 +/- 2.0 and 21.6 +/- 2.3; superficial white gastrocnemius and vastus lateralis). Rates for four mixed muscles were intermediate, ranging between 32.3 and 37.3. Specific de novo synthesis rates exhibited a strong correlation (r = 0.986) with muscle section citrate synthase activity. Turnover rates (de novo synthesis rate/adenine nucleotide pool size) were highest in high oxidative muscle (0.82-1.06%/h), lowest in low oxidative muscle (0.30-0.35%/h), and intermediate in mixed muscle (0.44-0.55%/h). Our results demonstrate that differences in adenine nucleotide management among fiber types extends to the process of de novo adenine nucleotide synthesis.

Adenine Nucleotides↗
PubMed1983

Adenine metabolism in erythrocytes of patients with Duchenne muscular dystrophy.

The primarily metabolic defect in Duchenne muscular dystrophy (DMD) is still unknown. In addition to the disturbance of muscle cell and erythrocyte membranes of patients with DMD an impairment of purine metabolism has been suggested on the basis of the decreased ATP content of the muscle fibers. To avoid the leakage of adenine nucleotides from cells, allopurinol has been administered to DMD patients to increase the formation of adenine nucleotides via the salvage pathway. The purpose of this study was to investigate this hypothesis of an effect of allopurinol on the formation of adenine nucleotides. Furthermore, the clinical status of allopurinol-treated DMD patients was examined. Biochemical studies were performed on erythrocytes of 19 patients with DMD, and adenine nucleotide concentrations and the incorporation of 14C-adenine into purine nucleotides were assessed before and after 6 months of allopurinol therapy. No improvement of the clinical status could be observed, although a slight increase in ATP formation was seen.

Adenine↗
PubMed1981

Adenine nucleotide levels of canine kidneys during hypothermic aerobic or anaerobic storage in Collins solution.

The influence of retrograde oxygen persufflation (ROP) on renal adenine nucleotide, glucose and lactate contents was examined in canine kidneys during up to 5 days of hypothermic preservation. Organs with or without predamage in 30-min normothermic ischemia were preserved and the results compared to kidneys after hypothermic ischemic storage (HIS): ROP preservation resulted in a significantly higher maintenance of cellular energy-rich substances than in HIS with even normal adenine nucleotide contents and energy charge potentials for the first 24 h. As in HIS preservation of normal kidneys, where the total adenine nucleotide content (SAN) paralleled the loss of viability for the first 1-2 days, in ROP were SAN and even the lactate content also correlated to renal viability for 2-3 days. But in contrast to this correlation, which would favor adenine nucleotide determinations for viability testing, in predamaged kidneys no correlation of SAN or lactate with renal viability was found during HIS or ROP. Thus the determination of cellular energy-rich adenine nucleotides and lactate accumulation confirms the superiority of ROP over HIS preservation. But the SAN or lactate tests lose their prognostic value for posttransplant renal viability if normothermic ischemia precedes the preservation period.

Adenine Nucleotides↗
PubMed1976

Effect of ischemia and infarction on regional content of adenine nucleotides and derivatives in canine left ventricle.

Samples of myocardium from four areas of ischemic and infarcted canine ventricle were examined over a 20-day period for content of the three adenine nucleotides as well as inosine, hypoxanthine, adenosine, and inosine monophosphate. The adenosine triphosphate (ATP) content of central and peripheral areas within the infarct fell to 11% and 8% of control, respectively, 1 day after coronary occlusion. The total adenine nucleotide (TAN) content in these areas fell to 17% of control and showed no significant recovery during the period of study. In the functional myocardium immediately surrounding the infarct the ATP content was depressed to 58% control after 1 day, and the TAN content was also depressed. In the healthy myocardium near the apex, the ATP content was significantly depressed only at the 3-day sample period. Adenine nucleotide derivatives were detected only at 30 min in the central ischemic area. The absence of the nucleoside and nucleobase compounds formed during adenine nucleotide degradation is attributed to their high membrane diffusibility. Loss of these compounds is considered a contributing factor in the prolonged depression of adenine nucleotide content in both ischemic and non-ischemic regions.

Adenine Nucleotides↗
PubMed1993

Reproductive insufficiency in the male rat with adenine-induced chronic renal failure.

The effect of adenine-induced chronic renal failure on the male reproductive system was studied using male Wistar rats. On the 30th experimental day, serum creatinine and urea nitrogen were elevated in adenine-treated rats. Body weight ratio of the testes and serum levels of gonadotropins (luteinizing hormone and follicle-stimulating hormone) in adenine-treated rats were similar to those in the controls. Serum testosterone level was reduced in adenine-induced uremic rats, but serum concentrations of 17 alpha-hydroxyprogesterone and androstenedione were increased in the uremic group. These results suggest that adenine-induced chronic renal failure reduces testicular function by suppressing 17 beta-hydroxysteroid oxidoreductase which converts androstenedione to testosterone.

17-alpha-Hydroxyprogesterone↗
PubMed1990

Beta-adrenergic stimulation of adenine nucleotide catabolism and purine release in human adipocytes.

The effects of beta-adrenergic agonists on ATP utilization and adenine nucleotide breakdown in human adipocytes were examined. The catecholamine-induced increase in cAMP was associated with an enhancement of adenine nucleotide catabolism resulting in an increase in release of inosine and hypoxanthine which can not be reutilized for adenine nucleotide synthesis. Therefore, one-third of total cellular adenine nucleotides were irreversibly lost in the presence of 1 mumol/liter isoproterenol. The catecholamine-induced increase in purine release could be blocked by phosphodiesterase inhibitors, suggesting that cAMP is the main precursor of purines in the presence of beta-adrenergic agonists. However, epinephrine (in the simultaneous presence of the alpha 2-adrenergic blocking agent, yohimbine) and isoproterenol were 10 times more potent in stimulating purine release than in elevating cAMP. In addition, purine release ceased when cAMP was still markedly increased, suggesting a compartmentation of the cyclic nucleotide and/or involvement of the hormone-sensitive, low Km cAMP phosphodiesterase. The results document that white fat cells have an enormous potential for dissipating energy, and demonstrate that the pathway involving cAMP formation and hydrolysis constitutes the principle route of adenine nucleotide catabolism in the presence of beta-adrenergic agonists.

1-Methyl-3-isobutylxanthine↗
PubMed2004

The exceptionally high rate of spontaneous mutations in the polymerase delta proofreading exonuclease-deficient Saccharomyces cerevisiae strain starved for adenine.

BACKGROUND: Mutagenesis induced in the yeast Saccharomyces cerevisiae by starvation for nutrilites is a well-documented phenomenon of an unknown mechanism. We have previously shown that the polymerase delta proofreading activity controls spontaneous mutagenesis in cells starved for histidine. To obtain further information, we compared the effect of adenine starvation on mutagenesis in wild-type cells and, in cells lacking the proofreading activity of polymerase delta (phenotype Exo-, mutation pol3-01). RESULTS: Ade+ revertants accumulated at a very high rate on adenine-free plates so that their frequency on day 16 after plating was 1.5 x 10(-4) for wild-type and 1.0 x 10(-2) for the Exo- strain. In the Exo- strain, all revertants arising under adenine starvation are suppressors of the original mutation, most possessed additional nutritional requirements, and 50% of them were temperature sensitive. CONCLUSIONS: Adenine starvation is highly mutagenic in yeast. The deficiency in the polymerase delta proofreading activity in strains with the pol3-01 mutation leads to a further 66-fold increase of the rate of mutations. Our data suggest that adenine starvation induces genome-wide hyper-mutagenesis in the Exo- strain.

Adenine↗
PubMed1979

Insulin release and metabolism of calcium, adenine and adenosine 3',5'-cyclic monophosphate.

In order to assess further the mechanisms involved in insulin release, we prelabeled rat pancreatic islets of Langerhans by incubating either 45Ca or [2-3H]adenine. When prelabeled islets were perfused with a glucose-free medium (the experiment with 45Ca) and a medium containing 2.8 mM glucose (the experiment with [2-3H]adenine) respectively, a constant rate of efflux of the radioactivity was established by 30 min in each case. D-Glucose at 16.7 mM concentration elicited a rapid efflux of 45Ca and [2-3H]adenine derivatives ([3H]Ad) within 4 to 6 min after commencing the step-wise stimulation by glucose, concomitantly with insulin release. However, L-glucose and D-galactose littel stimulated both 45Ca and [3H]Ad release. Lanthanum chloride caused a burst peak of 45Ca release in the absence of glucose. A rapid efflux of 45Ca was caused by beta-D-glucose and D-glyceraldehyde to much lesser extent than by alpha-D-glucose. The slowly rising concentration of glucose at 0.1 mM/min of gradient level failed to elicit any rapid efflux of 45Ca or [3H]Ad, although insulin release occurred in accordance with an increase in glucose concentration. Even when the gradient of glucose concentration was raised to 0.7 mM/min, glucose failed to stimulate an efflux of [3H]Ad but the subsequent stimulation by 16.7 mM glucose caused a rapid efflux of [3H]Ad concomitantly with the release of insulin. No rapid efflux of 45Ca was observed under a slow-rise glucose stimulation until the gradient level of the glucose concentration was raised to 6.7 mM. Analysis of distribution of the radioactive adenine derivatives after incubation showed that the adenosine fraction had the highest radioactivity in the medium followed by the ATP, adenine and cAMP fraction in that order, and the ATP fraction had the highest radioactivity in the islet. The ratio of radioactivity in the cAMP fraction in the medium to the total count was the highest among all. On the basis of these results, it was suggested that the discharge of [3H]Ad and 45Ca might occur with the alteration of the membrane permeability induced by a rapid change of the glucose concentration, and that their discharge might perhaps link to the glucoreceptor mechanism directly controlling insulin release.

Adenine↗
PubMed2006

A novel electrochemical biosensor for the detection of uric acid and adenine.

A novel electrochemical biosensor for the detection of uric acid and adenine was prepared based on a gel containing multi-walled carbon nanotubes and room-temperature ionic liquid of 1-octyl-3-methylimidazolium hexafluorophosphate. The electrochemistry of uric acid and adenine was studied in this gel modified electrode. There was a significant two-way electrocatalytic activity upon both oxidation and reduction of uric acid. Similar to a bare glassy carbon electrode, uric acid undergoes a 2e,2H+ oxidation in phosphate buffer in the modified electrode. A diimine, the oxidation product of uric acid, was found to be an unstable intermediate, which was converted by a follow-up hydration reaction to an imine alcohol, with the reaction rate constant of 8.5 +/- 0.3 M(-1).s(-1) according to Nicholson's theory. Under optimum conditions, linear calibration graphs were obtained over the concentration range of 1.0 x 10(-7) M approximately 1.0 x 10(-5) M (uric acid) and 1.0 x 10(-5) M approximately 6.0 x 10(-4) M (adenine). Based on the signal-to-noise ratio of 3, the detection limits of the current technique was found to be as low as 9.0 x 10(-8) M (uric acid) and 2.0 x 10(-6) M (adenine), respectively. This novel biosensor was successfully applied for the assay of uric acid in human urine. Because of its good stability and long-term durability, such a gel modified electrode can provide a simple and easy approach for sensitive detection of uric acid and adenine.

Adenine↗
PubMed1992

Ionization of adenine derivatives: EPR and ENDOR studies of X-irradiated adenine.HCl.1/2H2O and adenosine.HCl.

Following X irradiation of adenine.HCl.H2O at 10 K, evidence for five distinct radical products was present in the EPR/ENDOR. (In both adenine.HCl.1/2H2O and adenosine.HCl, the adenine base is present in a cationic form as it is protonated at N1). From ENDOR data, radical R1, stable at temperatures up to 250 K, was identified as the product of net hydrogen loss from N1. This product, evidently formed by electron loss followed by proton loss, is equivalent to the radical cation of the neutral adenine base. Radical R2, unstable at temperatures above 60 K, was identified as the product of net hydrogen addition to N3, and evidently formed by electron addition followed by proton addition. Radicals R3-R5 could not be identified with certainty. Similar treatment of adenosine.HCl provided evidence for six identifiable radical products. Radical R6, stable to ca. 150 K, was identified as the result of net hydrogen loss from the amino group, and evidently was the product of electron loss followed by proton loss. Radical R7 was tentatively identified as the product of net hydrogen addition to C4 of the adenine base. Radical R8 was found to be the product of net hydrogen addition to C2 of the adenine base, and R9 was the product of net hydrogen addition to C8. Radical R10 was identified as the product of net hydrogen abstraction from C1' of the ribose, and R11 was an alkoxy radical formed from the ribose. With the exception of R11, all products were also found following irradiation at 65 K. Only radical R8 and R9 were stable at room temperature. Most notable is the different deprotonation behavior of the primary electron-loss products (radical R1 vs. R6) and the different protonation behavior of the primary electron-gain products (radical R2 vs. no similar product in adenosine.HCl). The major structural difference in the two crystals is the electrostatic environment of the adenine base. Therefore, this study provides further evidence that environmental influences are important in determining proton transfer processes.

Adenine↗
PubMed2005

Effects of the Chinese herbal medicine based on Hachimi-jio-gan in male rats with the adenine-induced osteopenia.

In the adenine-induced renal failure rats, reversibility of renal failure and recovery of bone mineral density (BMD) by discontinuation of adenine-rich diet were reported. We think that the effect to bone metabolism with medication may be able to be evaluated as reinforcement of the BMD recovery. We have so far investigated the Chinese herbal medicine based on Hachimi-jio-gan (HJG) which are more effective than HJG alone. In this study, we investigated the effects of our Chinese herbal prescription on BMD in the adenine-treated rats compared to that of vitamin D3 treatment. Young male rats were administrated 100 mg/ml adenine for 8 weeks, and they showed renal failure and bone loss. The adenine-treated rats were divided into the following 3 groups, that is, the group experienced no treatment (control), the group given our Chinese herbal medicine (HAO), and the group given vitamin D3 (VD3) medication. It is likely that VD3 medication was less effective for increase of the femoral BMD than increase of the spinal BMD. In contrast, HAO was effective for increase of the femoral BMD. The VD3 group showed low deoxypyridinoline (Dpd: bone resorption maker) as compared to the control group. However, the HAO group showed same or slightly high Dpd. It is suggested that VD3 may increase BMD by reduction of bone resorption, while HAO may show effect on BMD by activating bone metabolism. It is indicated that HAO may become a curative medicine for bone loss because of the different target site from vitamin D3.

Adenine↗
PubMed1991

Effect of propionyl carnitine on energy charge and adenine nucleotide content of cardiac endothelial cells during hypoxia.

Adenine mucleotide metabolism is very active in endothelial cells. These cells are very rich in xanthine oxidase which may produce oxygen reactive species during ischaemia and reperfusion when a high amount of adenine nucleotides may be catabolized to hypoxanthine. We investigated the effect of propionyl carnitine on energy charge and nucleotide content in cultured endothelial cells during changes in oxygen partial pressure. During hypoxia the adenine nucleotide pool and the energy charge decreased more slowly in the presence of 0.5 mM propionyl carnitine than in the absence of the compound. Furthermore during reoxygenation a more rapid increase of energy charge and adenine nucleotide concentration was observed with propionyl carnitine. These observations suggest that the presence of propionyl carnitine allows the endothelial cells to maintain their functionality and regulatory role on vessel activity for a longer time and decreases the formation of oxygen reactive species due to xanthine oxidase activity on hypoxanthine formed by adenine nucleotide catabolism.

Adenine↗
PubMed1979

Inhibition of adenylate cyclase in human blood platelets by 9-substituted adenine derivatives.

A series of 9-substituted adenine derivatives inhibited adenylate cyclase activity (ATP pyrophosphate-lyase (cyclizing) EC 4.6.1.1) of a particulate preparation of human blood platelets. A 3--6 fold elevation of adenylate cyclase activity by prostaglandin E1 (PGE1) was inhibited in a concentration-related manner by 9-(tetrahydro-5-methyl-2-furyl) adenine (SQ 22,538), 9-(tetrahydro-2-furyl) adenine (SQ 22,536), 9-cyclopentyladenine (SQ 22,534), 9-furfuryladenine (sQ 4647) and 9-benzyladenine (SQ 218611). The I50 values ranged from 21 microM for SQ 22,538 to 140 microM for SQ 21,611. These same adenine derivatives reversed the inhibition by PGE1 of ADP-induced aggregation and the PGE1-stimulated elevation of adenosine 3':5'-monophosphate (cyclic AMP). The reversal of platelet aggregation inhibition by SQ 22,536 and SQ 4647 was concentration-related with I50 values of 30 microM in each case, whereas SQ 22,534 and SQ 21,611 reversed inhibition by 30% at 100 microM. SQ 22,536, SQ 22,534 and SQ 21,611 also blocked the increase in cyclic AMP levels in a concentration-related manner with I50 values of 1, 4 and 60 microM, respectively. SQ 4647 inhibited the elevation of cyclic AMP by more than 85% at 1000 microM. The adenine derivatives had no effect on platelet aggregation or on cyclic AMP levels in the absence of PGE1. These results provide additional evidence that the inhibition of platelet aggregation by PGE1 is mediated by cyclic AMP.

Adenine↗
PubMed1983

Isoosmotic sucrose, adenine, inosine media for preservation of blood.

In order to manipulate red cells to remove additives and metabolites prior to transfusion after prolonged preservation, osmotic fragility must be depressed. In isoosmotic sucrose solutions, the osmotic hemolysis curve is shifted to the left (less fragile) within several hours at 37 degrees C and within several days at 4 degrees C. However, hyperosmolar solution induced hemolysis when 0.9% NaCl was added after preservation. In isoosmotic sucrose solutions, the order of effectiveness in maintaining intracellular ATP content was: adenine plus inosine greater than inosine alone greater than adenine alone greater than no addition. The same order was also seen in depression of the increase in osmotic fragility during storage for 8 weeks. Formation of too stable erythrocytes to osmotic fragility and accordingly too low filtrability was prevented by the addition of appropriate amounts of physiological saline. Media containing isotonic sucrose, adenine and inosine depressed the increase in osmotic fragility during preservation for 6 weeks at 4 degrees C. ATP and 2,3-DPG levels were also better maintained than in various media containing a small amount of adenine. This finding with the former which indicated that the media containing isoosmotic sucrose, adenine and inosine prolonged posttransfusional viability of rabbit cells very much, suggests that these media are worthy of further investigation, since excess metabolites can be easily removed before transfusion.

2,3-Diphosphoglycerate↗
PubMed1984

Interaction among the distinct effects of adenine and guanine depletion in mouse lymphoma cells.

Toxic guanine depletion was shown previously to result in a dramatic reduction of DNA synthesis, while toxic adenine depletion failed to affect DNA synthesis (M. B. Cohen and W. Sadée, Cancer Res., 43: 1587-1591, 1983). In this study, relative DNA synthesis rates were measured in mouse lymphoma S49 cells over 24 hr after drug exposure and were compared to cell growth curves. DNA synthesis inhibition by mycophenolic acid (guanine starvation) was achieved at lower drug concentrations than was the inhibition of cell growth. This result further supports the hypothesis (reference above) that guanine starvation specifically affects cells in S phase while it allows cells with full DNA complement to divide. In contrast, L-alanosine (adenine starvation) failed to affect DNA synthesis for at least 24 hr at a concentration that inhibits cell growth by 80%. The dramatically different effects of guanine and adenine starvation on DNA synthesis can thus be used to assess the magnitude of each when blocking early de novo purine biosynthesis by 6-methyl-mercaptopurine ribonucleoside (6- MMPR ). The results suggest that, although 6- MMPR effects primarily resemble those of guanine depletion, adenine starvation measurably contributes to the overall toxicity of 6- MMPR . Drug combination experiments with L-alanosine, mycophenolic acid, and 6- MMPR suggest that the basic mechanisms underlying the toxic effects of guanine and adenine starvation act synergistically.

Adenine↗
PubMed1980

Hepatotrophic effects of insulin on glucose, glycogen, and adenine nucleotides in hepatocytes isolated from fasted adult rats.

Previous evidence that portal blood insulin is an hepatotrophic factor led to this study of its effect on hepatocytes, isolated from fasted rats, in suspension culture. Control hepatocytes (C), noninsulin-treated, and those infused continuously at low (LI) and high (HI) levels of insulin were compared concurrently with regard to their survival, glucose transport, and intracellular concentrations of glucose, glycogen, and adenine nucleotides, over a 48-hr period of incubation. Low insulin was adjudged to be comparable to portal insulin concentrations in fasted animals and HI to those in fed animals. All hepatocytes had been depleted of glucose, glycogen, and adenine nucleotides at the start of the study by prior fasting of the rat. For the first 6 hr of culture, there was little difference between C, LI, and HI with reference to the above parameters. In contrast, after 48 hr of incubation, cell survival, as judged by the DNA content, was signficiantly lower in C compared with LI and HI. The transport of 3--0-[methyl-3H] D-glucose was also significantly lower in C compared with LI and HI. The higher uptakes in both LI and HI were reduced by phloridzin, which had little effect on C. Correspondingly, the intracellular glucose concentrations in C were significantly lower than the extracellular glucose concentrations in contrast to those in LI and HI, which were comparable. For intracellular concentrations of glycogen and adenine nucleotides, the results of LI and HI were amalgamated as they were not significantly different from each other at 48 hr. Upon analysis, glycogen values were significantly higher for insulin-treated cells. Similarly, the total adenine nucleotide p-ol (ATP + ADP + AMP) also was clearly higher in HI + LI than in C. These results indicate that contrary to findings in studies with the perfused liver that have been of a short-term nature, insulin is necessary in the longer term (greater than 12 hr) for maintaining the transport of glucose into hepatocytes; thereby insulin promotes the maintenance of intracellular glucose, glycogen, and adenine nucleotide concentrations, and also enhances cell survival.

Adenine Nucleotides↗