scholarly journals Effect of adenosine on the adenine nucleotide content and metabolism of hepatocytes

1975 ◽  
Vol 152 (3) ◽  
pp. 593-599 ◽  
Author(s):  
P Lund ◽  
N W Cornell ◽  
H A Krebs
Keyword(s):  
Time Course ◽  
Ketone Bodies ◽  
Adenine Nucleotide ◽  
Adenine Nucleotides ◽  
Adenosine Kinase ◽  
Urea Synthesis ◽  
O2 Consumption ◽  
Nucleotide Content ◽  
Adenosine Concentration ◽  
Glucose Formation

ADENOSINE (0.5 MM) added to hepatocyte suspensions increased the intracellular concentration of ATP and total adenine nucleotides within 60 min up to three-fold. 2. Adenosine at 0.5 mM inhibited gluconeogenesis from lactate by about 50%. At higher adenosine concentrations the inhibition was less. There was no strict parallelism between the time-course of the increase of the adenine nucleotide content and the time-course of the inhibition of gluconeogenesis from lactate. 3. Adenosine abolished the accelerating effects of oleate and dibutyryl cyclic AMP on gluconeogenesis from lactate. 4. Gluconeogenesis was no significant effect of adenosine with fructose, dihydroxyacetone or glycerol. With asparagine, adenosine caused anacceleration of glucose formation. 5. Adenosine incorporation into adenine nucleotides accounted for about 20% of the adenosine removal. 6. Inosine, hypoxanthine or adenine compared with adenosine gave relatively slight increases of adenine nucleotides. 7. Urea synthesis from NH4Cl under optimum conditions i.e. in the presence of ornithine, lactate and oleate, was also inhibited by adenosine. The inhibition increased with the adenosine concentration and was 65% at 4 mM-adenosine. Again there was no correlation between the degree of inhibition of urea synthesis and the increase in the adenine nucleotide content. 8. The basal O2 consumption, the increased O2 consumption on the addition of oleate and the rate of formation of ketone bodies were not affected by the addition of adenosine. The [β-hydroxybutyrate]/[acetoacetate] ratio was increased by adenosine, provided that lactate was present. 9. The increase of the adenine nucleotide content of the hepatocytes on the addition of adenosine may be explained on the assumption that adenosine kinase is not regulated by feedback but by substrate supply.

scholarly journals L-Arginine Intake Effect on Adenine Nucleotide Metabolism in Rat Parenchymal and Reproductive Tissues

2012 ◽  
Vol 2012 ◽  
pp. 1-4 ◽  
Author(s):  
G. Kocic ◽  
J. Nikolic ◽  
T. Jevtovic-Stoimenov ◽  
D. Sokolovic ◽  
H. Kocic ◽  
...  
Keyword(s):  
Adenosine Deaminase ◽  
Adenine Nucleotide ◽  
Adenine Nucleotides ◽  
Tissue Growth ◽  
Nucleotide Metabolism ◽  
Amp Deaminase ◽  
Male Impotence ◽  
Adenine Nucleotide Metabolism ◽  
Adenosine Concentration ◽  
Male Wistar Rats

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 activities of the adenosine-producing enzyme,5′-NU and the adenosine-degrading enzyme-ADA adenosine deaminase. Dietary L-arginine intake directed adenine nucleotide metabolism in liver, kidney, and testis tissue toward the activation of adenosine production, by increased5′-NU activity and decreased ADA activity. Stimulation of adenosine accumulation could be of importance in mediating arginine antiatherosclerotic, vasoactive, immunomodulatory, and antioxidant effects. Assuming that the XO activity reflects the rate of purine catabolism in the cell, while the activity of AMP deaminase is of importance in ATP regeneration, reduced activity of XO, together with the increased AMP-deaminase activity, may suggest that adenine nucleotides are presumably directed to the ATP regenerating process during dietary L-arginine intake.

When does the lung die?K fc, cell viability, and adenine nucleotide changes in the circulation-arrested rat lung

1997 ◽  
Vol 83 (1) ◽  
pp. 247-252 ◽  
Author(s):  
David R. Jones ◽  
Randy M. Becker ◽  
Steve C. Hoffmann ◽  
John J. Lemasters ◽  
Thomas M. Egan
Keyword(s):  
Cell Viability ◽  
Time Course ◽  
Ischemia Reperfusion Injury ◽  
Adenine Nucleotide ◽  
Adenine Nucleotides ◽  
Ischemia Reperfusion ◽  
Rat Lung ◽  
Donor Pool ◽  
Ischemic Time

Jones, David R., Randy M. Becker, Steve C. Hoffmann, John J. Lemasters, and Thomas M. Egan. When does the lung die? K fc, cell viability, and adenine nucleotide changes in the circulation-arrested rat lung. J. Appl. Physiol. 83(1): 247–252, 1997.—Lungs harvested from cadaveric circulation-arrested donors may increase the donor pool for lung transplantation. To determine the degree and time course of ischemia-reperfusion injury, we evaluated the effect of O2 ventilation on capillary permeability [capillary filtration coefficient ( K fc)], cell viability, and total adenine nucleotide (TAN) levels in in situ circulation-arrested rat lungs. K fc increased with increasing postmortem ischemic time ( r = 0.88). Lungs ventilated with O2 1 h postmortem had similar K fc and wet-to-dry ratios as controls. Nonventilated lungs had threefold ( P < 0.05) and sevenfold ( P < 0.0001) increases in K fc at 30 and 60 min postmortem compared with controls. Cell viability decreased in all groups except for 30-min postmortem O2-ventilated lungs. TAN levels decreased with increasing ischemic time, particularly in nonventilated lungs. Loss of adenine nucleotides correlated with increasing K fc values ( r = 0.76). This study indicates that lungs retrieved 1 h postmortem may have normal K fc with preharvest O2 ventilation. The relationship between K fc and TAN suggests that vascular permeability may be related to lung TAN levels.

Regulation of hepatic gluconeogenesis in newborn rabbit: controlling factors in presuckling period

1985 ◽  
Vol 249 (5) ◽  
pp. E498-E505 ◽  
Author(s):  
W. A. Brennan ◽  
J. R. Aprille
Keyword(s):  
Adenine Nucleotide ◽  
Adenine Nucleotides ◽  
Mitochondrial Protein ◽  
Fold Increase ◽  
Insulin Injection ◽  
Pyruvate Carboxylation ◽  
Glucose Levels ◽  
Newborn Rabbit ◽  
Nucleotide Content

We have previously shown (Comp. Biochem. Physiol. 77B: 35-39, 1984) that a rapid postnatal increase in hepatic mitochondrial adenine nucleotide content activates pyruvate carboxylation and gluconeogenesis in the newborn rabbit. This study investigated factors limiting flux through the gluconeogenic pathway and examined the physiological stimuli responsible for the activation phenomenon. There is a 2.3-fold increase in total mitochondrial adenine nucleotides, along with a threefold increase in the matrix ATP/ADP ratio, by 2 h after birth, resulting overall in a sixfold increase in the amount of ATP/mg mitochondrial protein. Analysis of gluconeogenic intermediates, measured in freeze-clamped livers between birth and 4 h postnatal, suggests that pyruvate carboxylase controls gluconeogenic flux during this period. Newborn rabbits reared in an hypoxic environment (5% O2) exhibited decreased mitochondrial adenine nucleotide content, decreased rates of pyruvate carboxylation, and depressed blood glucose levels compared with littermates reared in room air or 95% O2. Manipulation of the insulin-to-glucagon ratio in vivo by injecting insulin at birth significantly delayed postnatal increases in the mitochondrial adenine nucleotide content and the rate of pyruvate carboxylation. Conversely, glucagon injection produced a supranormal increase in both mitochondrial adenine nucleotide content and pyruvate carboxylation. In addition, insulin injection prevented, whereas glucagon enhanced, the normal postnatal increase in tissue ATP/ADP. These results suggest that tissue oxygenation and a decreased insulin-to-glucagon ratio promote the rapid influx of adenine nucleotides from the liver cytosol into the mitochondrial matrix, thereby activating pyruvate carboxylation and gluconeogenesis during the presuckling period.

The effects of adenine nucleotide perfusion on interstitial adenosine production in rat skeletal muscle

2018 ◽  
Vol 96 (8) ◽  
pp. 823-829
Author(s):  
Yi Zhao ◽  
Sergio Fabris ◽  
David A. MacLean
Keyword(s):  
Skeletal Muscle ◽  
Muscle Contraction ◽  
Adenine Nucleotide ◽  
Adenine Nucleotides ◽  
Interstitial Space ◽  
Rat Skeletal Muscle ◽  
Adenosine Concentration

The purpose of the present study was to utilize the microdialysis technique in rat skeletal muscle to perfuse varying concentrations of AMP, ADP, and ATP into the interstitium to examine the effects that these adenine nucleotides have on the production of adenosine in the interstitial space. Interstitial adenosine production appears to be related to the type (ATP, ADP, or AMP) and concentration (2–60 μmol/L) of the adenine nucleotide perfused. Interstitial adenosine levels increased (P < 0.05) from baseline (0.18 ± 0.02 and 0.22 ± 0.02 μmol/L) to 0.23 ± 0.02 and 0.41 ± 0.05 μmol/L following 5 and 30 μmol/L AMP perfusion, respectively. Similarly, perfusion with 30 μmol/L ADP and 30, 40, and 60 μmol/L ATP resulted in an increase (P < 0.05) in interstitial adenosine concentration from baseline (0.25 ± 0.02, 0.26 ± 0.02, 0.19 ± 0.03, and 0.14 ± 0.02 μmol/L) to 0.30 ± 0.02, 0.32 ± 0.02, 0.36 ± 0.04, and 0.33 ± 0.04 μmol/L, respectively. Interestingly, the most prominent increase in interstitial adenosine production occurred during the perfusion of 60 μmol/L ATP (126% increase from baseline). These data strongly suggest that interstitial ATP may play a more potent role in stimulating interstitial adenosine production as compared with ADP or AMP. In addition, interstitial adenosine production can occur independent of muscle contraction (voluntary or involuntary) or hypoxia when adequate concentrations of adenine nucleotides are available.

scholarly journals Changes in Levels of Nicotinamide Adenine Nucleotides and Krebs Cycle Intermediates in Mung Bean Leaves after Illumination

1967 ◽  
Vol 20 (2) ◽  
pp. 319 ◽  
Author(s):  
D Graham ◽  
Judith E Cooper
Keyword(s):  
Nicotinamide Adenine Dinucleotide ◽  
Time Course ◽  
Adenine Nucleotide ◽  
Adenine Nucleotides ◽  
Krebs Cycle ◽  
Nicotinamide Adenine Dinucleotide Phosphate ◽  
Nicotinamide Adenine ◽  
Rapid Decline ◽  
Second Phase ◽  
Krebs Cycle Intermediates

Changes in levels of nicotinamide adenine nucleotides were measured during a short (30 min) period of illumination following a dark period. Two phases in the time course were found. In the first phase, during the first minute of illumination, a rapid decline in oxidized nicotinamide adenine dinucleotide occurred which represented a net loss of nicotinamide adenine nucleotide. In the subsequent, second phase during illumination, a slower decline in oxidized nicotinamide adenine dinucleotide was found which was coincident with increases in nicotinamide adenine dinucleotide phosphate(s). The changes in the reduced nicotinamide adenine nucleo� tides were relatively small during illumination.

Adenine Nucleotides in Platelets from Normal and Uraemic Subjects

1968 ◽  
Vol 19 (01/02) ◽  
pp. 036-040 ◽  
Author(s):  
W. R Pitney ◽  
H Hinterberger ◽  
M Potter
Keyword(s):  
Glass Bead ◽  
Adenine Nucleotide ◽  
Adenine Nucleotides ◽  
Blood Samples ◽  
Nucleotide Content ◽  
Before And After

SummaryAdenine nucleotides in platelets from normal and uraemic subjects were measured before and after passage of blood through glass bead filters. Platelets from uraemic subjects contained normal amounts of ATP, ADP, AMP and total nucleotides. Normal platelets which had passed through filters contained higher concentrations of ATP, ADP and total nucleotides than platelets in control blood samples, indicating either heterogeneity of adenine nucleotide content in normal platelets or possibly adsorption of nucleotides onto platelets during their passage through the filters. This phenomenon was not observed with platelets from uraemic patients.

Adenosine metabolism in human skin fibroblasts

1985 ◽  
Vol 248 (1) ◽  
pp. C21-C26 ◽  
Author(s):  
M. J. Holland ◽  
E. Murphy ◽  
J. K. Kelleher
Keyword(s):  
Initial Rate ◽  
Adenine Nucleotide ◽  
Adenine Nucleotides ◽  
Product Formation ◽  
Human Skin Fibroblasts ◽  
Metabolic Fate ◽  
Normal Cells ◽  
Extracellular Adenosine ◽  
Adenosine Concentration ◽  
The Media

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 considerably lower in adenosine deaminase (ADA)-deficient cells than in normal cells and virtually eliminated in normal cells by the presence of 1 microM deoxycoformycin (a potent ADA inhibitor), suggesting that labeled inosine and hypoxanthine production requires ADA activity. Initial rates of deamination (inosine and hypoxanthine formation) and phosphorylation (adenine nucleotide formation) were estimated by examining the metabolic fate of [8-14C]adenosine in hypoxanthine phosphoribosyltransferase-deficient cells, which cannot recycle hypoxanthine. The estimate of the initial rate of phosphorylation exceeded that of deamination only at the lowest adenosine concentration examined (0.25 microM). The ratio of deamination to phosphorylation rose from approximately 1 at 0.41 microM to approximately 15 at 400 microM extracellular adenosine.

scholarly journals Fuel utilization in colonocytes of the rat

1985 ◽  
Vol 231 (3) ◽  
pp. 713-719 ◽  
Author(s):  
M S M Ardawi ◽  
E A Newsholme
Keyword(s):  
Colonic Mucosa ◽  
Ketone Bodies ◽  
Adenine Nucleotides ◽  
Maximum Activity ◽  
Glutamine Metabolism ◽  
O2 Consumption ◽  
Fructose Bisphosphatase ◽  
Fuel Utilization ◽  
Donor Animal ◽  
End Products

In incubated colonocytes isolated from rat colons, the rates of utilization O2, glucose or glutamine were linear with respect to time for over 30 min, and the concentrations of adenine nucleotides plus the ATP/ADP or ATP/AMP concentration ratios remained approximately constant for 30 min. Glutamine, n-butyrate or ketone bodies were the only substrates that caused increases in O2 consumption by isolated incubated colonocytes. The maximum activity of hexokinase in colonic mucosa is similar to that of 6-phosphofructokinase. Starvation of the donor animal decreased the activities of hexokinase and 6-phosphofructokinase, whereas it increased those of glucose-6-phosphatase and fructose-bisphosphatase. Isolated incubated colonocytes utilized glucose at about 6.8 mumol/min per g dry wt., with lactate accounting for 83% of glucose removed. These rates were not affected by the addition of glutamine, acetoacetate or n-butyrate, and starvation of the donor animal. Isolated incubated colonocytes utilized glutamine at about 5.5 mumol/min per g dry wt., which is about 21% of the maximum activity of glutaminase. The major end-products of glutamine metabolism were glutamate, aspartate, alanine and ammonia. Starvation of the donor animal decreased the rate of glutamine utilization by colonocytes, which is accompanied by a decrease in glutamate formation and in the maximum activity of glutaminase. Isolated incubated colonocytes utilized acetoacetate at about 3.5 mumol/min per g dry wt. This rate was not markedly affected by addition of glucose or by starvation of the donor animal. When colonocytes were incubated with n-butyrate, both acetoacetate and 3-hydroxybutyrate were formed, with the latter accounting for only about 19% of total ketones produced.

Prolonged adenine nucleotide resynthesis and reperfusion injury in postischemic skeletal muscle

1992 ◽  
Vol 262 (5) ◽  
pp. H1538-H1547 ◽  
Author(s):  
B. B. Rubin ◽  
S. Liauw ◽  
J. Tittley ◽  
A. D. Romaschin ◽  
P. M. Walker
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Time Course ◽  
Adenine Nucleotide ◽  
Adenine Nucleotides ◽  
Prolonged Release ◽  
Intracellular Acidosis ◽  
Edema Formation ◽  
Muscle Necrosis

Skeletal muscle ischemia results in energy depletion and intracellular acidosis. Reperfusion is associated with impaired adenine nucleotide resynthesis, edema formation, and myocyte necrosis. The purpose of these studies was to define the time course of cellular injury and adenine nucleotide depletion and resynthesis in postischemic skeletal muscle during prolonged reperfusion in vivo. The isolated canine gracilis muscle model was used. After 5 h of ischemia, muscles were reperfused for either 1 or 48 h. Lactate and creatine phosphokinase (CPK) release during reperfusion was calculated from arteriovenous differences and blood flow. Adenine nucleotides, nucleosides, bases, and creatine phosphate were quantified by high-performance liquid chromatography, and muscle necrosis was assessed by nitroblue tetrazolium staining. Reperfusion resulted in a rapid release of lactate, which paralleled the increase in blood flow, and a delayed but prolonged release of CPK. Edema formation and muscle necrosis increased between 1 and 48 h of reperfusion (P less than 0.05). Recovery of energy stores during reperfusion was related to the extent of postischemic necrosis, which correlated with the extent of nucleotide dephosphorylation during ischemia (r = 0.88, P less than 0.001). These results suggest that both adenine nucleotide resynthesis and myocyte necrosis, which are protracted processes in reperfusing skeletal muscle, are related to the extent of nucleotide dephosphorylation during ischemia.

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