Hydrogen peroxide, an inhibitor of platelet function: Effect on adenine nucleotide metabolism, and the release reaction

1977 ◽  
Vol 2 (1) ◽  
pp. 53-63 ◽  
Author(s):  
Marie J. Stuart ◽  
Holm Holmsen
Keyword(s):  
Hydrogen Peroxide ◽  
Platelet Function ◽  
Adenine Nucleotide ◽  
Nucleotide Metabolism ◽  
Release Reaction ◽  
Adenine Nucleotide Metabolism

Studies on the Platelet Defect in Alcoholism

1975 ◽  
Vol 33 (02) ◽  
pp. 310-327 ◽  
Author(s):  
Dale H Cowan ◽  
Richard C Graham
Keyword(s):  
Platelet Function ◽  
Adenine Nucleotide ◽  
Specific Radioactivity ◽  
Protein Composition ◽  
Nucleotide Metabolism ◽  
Supernatant Fraction ◽  
Release Mechanism ◽  
Adenine Nucleotide Metabolism ◽  
Thrombocytopenic Patient

SummaryPlatelet ultrastructure, protein composition, and adenine nucleotide metabolism were studied in patients ingesting ethanol to elucidate the mechanism of ethanol-induced changes in platelet function and survival. Serial measurements were made in 2 patients who maintained blood ethanol levels in excess of 300 mg/100 ml for 3 to 4 weeks. No major changes in structure or metabolism were detected in platelets from the patient whose platelet counts remained stable during the ingestion period. By contrast, the development of thrombocytopenia in the other patient was associated with significantly reduced intracellular ADP, increased ATP/ADP ratio, decreased release of ADP, increased specific radioactivity of intracellular ATP and ADP, and increased formation of hypoxanthine. Additionally, platelets from this patient varied markedly in size, contained giant granules, and possessed a poorly defined micro-tubular system. After stimulation with ADP or collagen, centripetal granule migration was retarded, and the aggregates formed were small and loose. Several large proteins were absent from the supernatant fraction of sonicated platelets from the thrombocytopenic patient. Exposure of normal platelets to ethanol in vitro resulted in no detectable change in platelet ultrastructure. The data indicate that the ethanol-related abnormalities of platelet function are due in part to subnormal amounts of intracellular ADP and a deficit in the storage pool of ADP. Additionally, the results suggest that impairment in the release mechanism to the observed defect in the release reaction.

scholarly journals The Effect of Cold on Platelets. III. Adenine Nucleotide Metabolism After Brief Storage at Cold Temperature

Blood ◽  
1973 ◽  
Vol 42 (4) ◽  
pp. 557-564 ◽  
Author(s):  
Herman E. Kattlove ◽  
Dorothy Mormino
Keyword(s):  
Connective Tissue ◽  
Prostaglandin E1 ◽  
Room Temperature ◽  
Adenine Nucleotide ◽  
Platelet Rich Plasma ◽  
Adenine Nucleotides ◽  
Nucleotide Metabolism ◽  
Immunoglobulin M ◽  
Release Reaction ◽  
Adenine Nucleotide Metabolism

Abstract The effect of cold on platelet adenine nucleotide (PAN) metabolism was studied. Spontaneous aggregation which occurs when chilled platelet-rich plasma (PRP) is simultaneously warmed and stirred was not accompanied by the changes in adenine nucleotides associated with the release reaction. Connective tissue caused the release of the same amount of ADP and conversion of equal amounts of ATP to IMP and hypoxanthine in cold-stored platelets as it did in room temperature stored platelets. However, cold did have an important effect on PAN. In PRP stored at cold (0° C, 3° C) temperatures and warmed up to 37° C in the presence of 3H adenine, there was an increase in the conversion of adenine to its metabolites and ultimately to hypoxanthine as compared to PRP stored at warmer temperatures. This effect could not be prevented by ouabain, prostaglandin E1, antibody to immunoglobulin M or adenosine.

scholarly journals The effect of platelet concentrate storage temperature on adenine nucleotide metabolism

Blood ◽  
1975 ◽  
Vol 45 (6) ◽  
pp. 749-756
Author(s):  
DJ Filip ◽  
JD Eckstein ◽  
CA Sibley
Keyword(s):  
Storage Temperature ◽  
Adenine Nucleotide ◽  
Nucleotide Metabolism ◽  
Platelet Concentrate ◽  
Release Reaction ◽  
C Storage ◽  
Adenine Nucleotide Metabolism ◽  
Red Cell Count ◽  
Ph Decrease ◽  
Adenine Nucleotide Pool

The effect of platelet concentrate storage temperature (4 degrees C versus 22 degrees C) on platelet adenine nucleotide metabolism was studied. In general, levels of platelet ATP and ADP, the release reaction, and the metabolis nucleotide pool were best preserved for 72 hr by storage of concentrates at 4 degrees C. Storage of concentrates for 72 hr at 22 degrees C was occasionally associated with a pH decrease to less than 6.0, which is incompatible with platelet viability. When the pH fell below 6.0, there was a marked deterioration of platelet adenine nucleotide levels and the release reaction. The results for concentrates stored at 22 degrees C, with a final pH above 6.0, were not inferior to the results for those stored at 4 degrees C. The pH remained above 7.0 in all concentrates stored at 4 degrees C. The pH changes of platelet concentrates stored at 22 degrees C could not solely be attributed to platelet count, red cell count, or bacterial contamination. Storage at both temperatures was associated with conversion of ATP in the metabolic adenine nucleotide pool to hypoxanthine.

scholarly journals Studies on the mechanism of ristocetin-induced platelet aggregation

Blood ◽  
1975 ◽  
Vol 45 (1) ◽  
pp. 91-96 ◽  
Author(s):  
HE Kattlove ◽  
MH Gomez
Keyword(s):  
Platelet Aggregation ◽  
Adenine Nucleotide ◽  
Nucleotide Metabolism ◽  
Release Reaction ◽  
Platelet Membranes ◽  
Adenine Nucleotide Metabolism ◽  
Induced Aggregation

Abstract Adenine nucleotide metabolism and the release reaction were studied during ristocetin-induced platelet aggregation. Decreasing platelet ATP by incubation with metabolic poisons did not decrease ristocetin- induced aggregation. ADP and ATP were released from platelets during ristocetin-induced aggregation, and ATP was converted to hypoxanthine. However, these occurred after aggregation was almost complete. Aggregation was inhibited by p-choromercuribenzoic acid. By studying platelet suspensions, we were able to determine that this effect was on platelets and not on the plasma cofactor needed for aggregation. We postulate that ristocetin and its cofactor aggregate platelets by binding platelet membranes and that the platelet plays a passive role in this reaction.

scholarly journals Studies on the mechanism of ristocetin-induced platelet aggregation

Blood ◽  
1975 ◽  
Vol 45 (1) ◽  
pp. 91-96
Author(s):  
HE Kattlove ◽  
MH Gomez
Keyword(s):  
Platelet Aggregation ◽  
Adenine Nucleotide ◽  
Nucleotide Metabolism ◽  
Release Reaction ◽  
Platelet Membranes ◽  
Adenine Nucleotide Metabolism ◽  
Induced Aggregation

Adenine nucleotide metabolism and the release reaction were studied during ristocetin-induced platelet aggregation. Decreasing platelet ATP by incubation with metabolic poisons did not decrease ristocetin- induced aggregation. ADP and ATP were released from platelets during ristocetin-induced aggregation, and ATP was converted to hypoxanthine. However, these occurred after aggregation was almost complete. Aggregation was inhibited by p-choromercuribenzoic acid. By studying platelet suspensions, we were able to determine that this effect was on platelets and not on the plasma cofactor needed for aggregation. We postulate that ristocetin and its cofactor aggregate platelets by binding platelet membranes and that the platelet plays a passive role in this reaction.

scholarly journals The effect of platelet concentrate storage temperature on adenine nucleotide metabolism

Blood ◽  
1975 ◽  
Vol 45 (6) ◽  
pp. 749-756 ◽  
Author(s):  
DJ Filip ◽  
JD Eckstein ◽  
CA Sibley
Keyword(s):  
Storage Temperature ◽  
Adenine Nucleotide ◽  
Nucleotide Metabolism ◽  
Platelet Concentrate ◽  
Release Reaction ◽  
C Storage ◽  
Adenine Nucleotide Metabolism ◽  
Red Cell Count ◽  
Ph Decrease ◽  
Adenine Nucleotide Pool

Abstract The effect of platelet concentrate storage temperature (4 degrees C versus 22 degrees C) on platelet adenine nucleotide metabolism was studied. In general, levels of platelet ATP and ADP, the release reaction, and the metabolis nucleotide pool were best preserved for 72 hr by storage of concentrates at 4 degrees C. Storage of concentrates for 72 hr at 22 degrees C was occasionally associated with a pH decrease to less than 6.0, which is incompatible with platelet viability. When the pH fell below 6.0, there was a marked deterioration of platelet adenine nucleotide levels and the release reaction. The results for concentrates stored at 22 degrees C, with a final pH above 6.0, were not inferior to the results for those stored at 4 degrees C. The pH remained above 7.0 in all concentrates stored at 4 degrees C. The pH changes of platelet concentrates stored at 22 degrees C could not solely be attributed to platelet count, red cell count, or bacterial contamination. Storage at both temperatures was associated with conversion of ATP in the metabolic adenine nucleotide pool to hypoxanthine.

The Platelet of the Newborn Infant – Adenine Nucleotide Metabolism and Release

1980 ◽  
Vol 43 (02) ◽  
pp. 099-103 ◽  
Author(s):  
J M Whaun ◽  
P Lievaart ◽  
Keyword(s):  
Newborn Infant ◽  
Adenine Nucleotide ◽  
Platelet Rich Plasma ◽  
Adenine Nucleotides ◽  
Newborn Infants ◽  
Specific Radioactivity ◽  
Nucleotide Metabolism ◽  
Breakdown Product ◽  
Term Infants ◽  
Adenine Nucleotide Metabolism

SummaryBlood from normal full term infants, mothers and normal adults was collected in citrate. Citrated platelet-rich plasma was prelabelled with 3H-adenine and reacted with release inducers, collagen and adrenaline. Adenine nucleotide metabolism, total adenine nucleotide levels and changes in sizes of these pools were determined in platelets from these three groups of subjects.At rest, the platelet of the newborn infant, compared to that of the mother and normal adult, possessed similar amounts of adenosine triphosphate (ATP), 4.6 ± 0.2 (SD), 5.0 ± 1.1, 4.9 ± 0.6 µmoles ATP/1011 platelets respectively, and adenosine diphosphate (ADP), 2.4 ± 0.7, 2.8 ± 0.6, 3.0 ± 0.3 umoles ADP/1011 platelets respectively. However the marked elevation of specific radioactivity of ADP and ATP in these resting platelets indicated the platelet of the neonate has decreased adenine nucleotide stores.In addition to these decreased stores of adenine nucleotides, infant platelets showed significantly impaired release of ADP and ATP on exposure to collagen. The release of ADP in infants, mothers, and other adults was 0.9 ± 0.5 (SD), 1.5 ± 0.5, 1.5 ± 0.1 umoles/1011 platelets respectively; that of ATP was 0.6 ± 0.3, 1.0 ± 0.1,1.3 ± 0.2 µmoles/1011 platelets respectively. With collagen-induced release, platelets of newborn infants compared to those of other subjects showed only slight increased specific radioactivities of adenine nucleotides over basal levels. The content of metabolic hypoxanthine, a breakdown product of adenine nucleotides, increased in both platelets and plasma in all subjects studied.In contrast, with adrenaline as release inducer, the platelets of the newborn infant showed no adenine nucleotide release, no change in total ATP and level of radioactive hypoxanthine, and minimal change in total ADP. The reason for this decreased adrenaline reactivity of infant platelets compared to reactivity of adult platelets is unknown.Infant platelets may have different membranes, with resulting differences in regulation of cellular processes, or alternatively, may be refractory to catecholamines because of elevated levels of circulating catecholamines in the newborn period.

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.

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