The relationship between the adenine nucleotide metabolism and the conversion of the xanthine oxidase enzyme system in ischemia-reperfusion of the rat small intestine

The relationship between changes in the muscle total adenine nucleotide pool (TAN = ATP + ADP + AMP) and IMP during and after 30 s of sprint cycling was examined. Skeletal muscle samples were obtained from the vastus lateralis muscle of seven untrained men (23.9 ± 2.3 yr, 74.4 ± 3.6 kg, and 55.0 ± 2.9 ml ⋅ kg−1 ⋅ min−1peak oxygen consumption) before and immediately after exercise and after 5 and 10 min of passive recovery. The exercise-induced increase in muscle IMP was linearly related to the decrease in muscle TAN ( r = −0.97, P < 0.01), and the slope of this relationship (−0.83) was not different from 1.0 ( P > 0.05), indicating a 1:1 stoichiometric relationship. This interpretation must be treated cautiously, because all subjects displayed a greater decrease in TAN compared with the increase in IMP content, and the TAN + IMP + inosine + hypoxanthine content was lower ( P < 0.05) immediately after exercise compared with during rest. During the first 5 min of recovery, the increase in TAN was not correlated with the decrease in IMP ( r = −0.18, P> 0.05). In all subjects, the magnitude of TAN increase was higher than the magnitude of IMP decrease over this recovery period. In contrast, the increase in TAN was correlated with the decrease in IMP throughout the second 5 min of recovery ( r = −0.80, P < 0.05), and it was a 1:1 stoichiometric relationship (slope = −1.12). These data indicate that a small proportion of the TAN pool was temporarily lost from the muscle purine stores during sprinting but was rapidly recovered after exercise.

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Programmed cell death induced by ischemia-reperfusion in rat intestinal mucosa

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.1998.274.2.g270 ◽

1998 ◽

Vol 274 (2) ◽

pp. G270-G276 ◽

Cited By ~ 36

Author(s):

Takahiro Noda ◽

Ryuichi Iwakiri ◽

Kazuma Fujimoto ◽

Shuzo Matsuo ◽

Tak Yee Aw

Keyword(s):

Small Intestine ◽

Mesenteric Artery ◽

Immunohistochemical Staining ◽

Ischemia Reperfusion ◽

Rat Small Intestine ◽

Halothane Anesthesia ◽

Fragmented Dna ◽

Ischemia Group ◽

Total Dna ◽

The Relationship

Apoptosis after ischemia-reperfusion (I/R) was characterized in rat small intestine. Under halothane anesthesia, the superior mesenteric artery in the rat was occluded for 15 or 60 min, followed by reperfusion. Ratios of fragmented DNA to total DNA, electrophoresis, and immunohistochemical staining were examined after I/R. Some rats were pretreated with α-difluoromethylornithine (DFMO) to examine the relationship between intestinal apoptosis and ornithine decarboxylase (ODC) activity. The percentage of fragmented DNA significantly increased just after ischemia and peaked at 1 h after reperfusion in the jejunum and ileum. These increases were significantly higher in the 60-min ischemia group compared with the 15-min ischemia group. This increase decreased 6 h after reperfusion. The results were corroborated by histological evaluations of the intestine under the same conditions. DFMO completely abolished elevation of ODC activity 6 h after reperfusion but did not change the percentage of fragmented DNA. Apoptosis in rat small intestine was induced by ischemia of the gut, and this process was exacerbated by reperfusion. The changes in apoptosis were independent of ODC activity.

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

Thrombosis and Haemostasis ◽

10.1055/s-0038-1650026 ◽

1980 ◽

Vol 43 (02) ◽

pp. 099-103 ◽

Cited By ~ 9

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.

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

The Scientific World JOURNAL ◽

10.1100/2012/208239 ◽

2012 ◽

Vol 2012 ◽

pp. 1-4 ◽

Cited By ~ 5

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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Release-induced changes in adenine nucleotide metabolism of human blood platelets

Thrombosis Research ◽

10.1016/0049-3848(79)90139-7 ◽

1979 ◽

Vol 15 (3-4) ◽

pp. 309-318 ◽

Cited By ~ 2

Author(s):

I. von Pusch ◽

W. Wesemann

Keyword(s):

Human Blood ◽

Adenine Nucleotide ◽

Blood Platelets ◽

Nucleotide Metabolism ◽

Adenine Nucleotide Metabolism ◽

Induced Changes ◽

Human Blood Platelets

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The relationship between concentration and uptake by rat small intestine, in vitro, for two micellar solutes

Biochimica et Biophysica Acta (BBA) - Biomembranes ◽

10.1016/0005-2736(71)90356-7 ◽

1971 ◽

Vol 233 (1) ◽

pp. 49-52 ◽

Cited By ~ 9

Author(s):

N.E. Hoffman ◽

V.J. Yeoh

Keyword(s):

Small Intestine ◽

Rat Small Intestine ◽

The Relationship

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The Murine Misty Mutation: Phenotypic Effects on Melanocytes, Platelets and Brown Fat

Genetics ◽

10.1093/genetics/148.1.381 ◽

1998 ◽

Vol 148 (1) ◽

pp. 381-390

Author(s):

Elena V Sviderskaya ◽

Edward K Novak ◽

Richard T Swank ◽

Dorothy C Bennett

Keyword(s):

Coat Color ◽

Adenine Nucleotide ◽

Primary Cultures ◽

Cell Types ◽

Nucleotide Metabolism ◽

Brown Fat ◽

Melanocyte Stimulating Hormone ◽

Prolonged Bleeding Time ◽

Adenine Nucleotide Metabolism

Abstract Although the recessive murine mutation misty (m) is well known, its phenotype has never been reported beyond brief descriptions of a dilution of coat color and white spotting of the belly and extremities, suggesting a developmental mutation. A report in abstract has also suggested effects on white fat and body weight. Here, we report effects of the homozygous misty mutation on an unusual combination of three cell types: melanocytes, platelets, and brown fat. Brown fat appeared to be completely absent from all expected locations in neonatal m/m mice. A prolonged bleeding time was observed; platelet count and platelet serotonin and ATP levels were normal, but the level of ADP in m/m platelets was low. Primary cultures and immortal lines of melanocytes from m/m mice showed several abnormalities. There was a marked deficiency in net proliferation, suggesting that the color dilution and spotting in vivo may result from reduced numbers of melanocytes and their precursors. m/m melanocytes were also hyperdendritic in morphology, overproduced melanin, and had deficient responses to the cAMP agonists cholera toxin and melanocyte-stimulating hormone, which normally promote melanin production. The misty gene product may be involved in adenine nucleotide metabolism or signaling.

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