Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P47989 (xanthine oxidase)
 8,633 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Adenosine and adenine nucleotides shorten the action potential duration of atrial myocytes and activate a specific acetylcholine and adenosine receptor-operated potassium outward current referred to as IKACh,Ado. The objective of this study was to determine whether adenine nucleotides shorten the action potential duration and increase IKACh,Ado in guinea pig atrial myocytes by directly activating adenosine receptors. The potency and efficacy of AMP and adenosine in increasing IKACh,Ado and shortening atrial action potential duration were similar; the EC50 values for AMP and adenosine were 3.4 +/- 0.8 and 3.1 +/- 0.4 microM, respectively. Likewise, the maximum increases in IKACh,Ado caused by AMP and adenosine were similar (122 +/- 11% versus 123 +/- 9%). In comparison, ATP and the stable analogue of AMP, adenosine monophosphorothioate (AMPS), were significantly less potent and efficacious than adenosine and AMP, and adenosine receptor antagonist 8-(p-sulfophenyl)theophylline and abolished in the presence of adenosine deaminase and alpha, beta-methylene-ADP (APCP, an inhibitor of AMP degradation). Binding of the A1-adenosine antagonist [3H]8-cyclopentyl-1,3-dipropylxanthine (DPCPX) to guinea pig atrial membranes treated with adenosine deaminase and APCP was reduced up to 60% by 100 microM concentrations of AMP, AMPS, and adenosine. Inosine inhibited binding by 43 +/- 3% at 100 microM, whereas hypoxanthine and xanthine had little (5-10% inhibition) and uric acid had no effect. Only 3% of AMP and 35% of AMPS were recovered intact after a 90-minute incubation at 21 degrees C with preparations of guinea pig atrial membranes. Percent displacement of [3H]DPCPX binding to atrial membranes by 100 microM AMP was significantly less in the presence of nucleoside phosphorylase and xanthine oxidase (to degrade inosine, hypoxanthine, and xanthine to uric acid) than in their absence (12.4 +/- 3.1% versus 49.7 +/- 1.5%). The results suggest that the observed electrophysiological actions of adenine nucleotides in cardiomyocytes are mediated by adenosine and are consistent with activation of A1-adenosine receptors.
 ...
PMID:Electrophysiological and receptor binding studies to assess activation of the cardiac adenosine receptor by adenine nucleotides. 200 6

1. Adenosine metabolizing enzymes in seminal plasma of man and bull have been investigated. 2. A different level of 5'-nucleotidase activity has been found in two seminal plasmas: in bull 5'-nucleotidase represents 80% of the total AMP dephosphorylating enzymes while in man 5'-nucleotidase represents only 1.3% of the total AMP dephosphorylating activities. 3. Apart from the different levels of 5'-nucleotidase activity, different kinetic parameters have been reported for 5'-nucleotidase, acid prostatic phosphatases, ADA and PNP. 4. Adenosine kinase, xanthine oxidase and AdoHcy-hydrolase have not been detected in the seminal plasma of man and bull.
 ...
PMID:Adenosine metabolizing enzymes in seminal plasma of bull and man: a comparative study. 212 26

Acetylcholine and ATP are costored and coreleased during synaptic activity at the electric organ of Torpedo. It has been suggested that released ATP is converted to adenosine at the synaptic cleft, and in turn this nucleoside would depress the evoked release of acetylcholine. In the present communication we have used a chemiluminescent reaction that let us to monitor continuously the presence of adenosine in this preparation. The chemiluminescent reaction is based on the conversion of adenosine into uric acid and H2O2 by adenosine deaminase, nucleoside phosphorylase, and xanthine oxidase enzymes. The hydrogen peroxide has been detected by peroxidase-luminol mixture. The reaction has a sensitivity on the picomol range and discerned between Adenosine, AMP, ADP, and ATP. We have developed this technique in the hope of understanding whether adenosine is released during synaptic activity or it comes from the released ATP. We have studied the release or formation of adenosine in fragments of the electric organ and in isolated cholinergic nerve terminals obtained from it. In both conditions we have followed the effect of potassium stimulation upon the detection of adenosine. Potassium stimulation increased the extracellular adenosine either in slices or the synaptosomal fraction of Torpedo electric organ. The presence of alpha, beta-methylene ADP, an inhibitor of 5'-nucleotidase, inhibits the detection of adenosine, suggesting that extracellular adenosine is a consequence of ectocellular dephosphorylation of released ATP.
 ...
PMID:The release of adenosine at the electric organ of Torpedo. A study using a continuous chemiluminescent method. 232 27

An in vivo rat hindlimb tourniquet ischemia model was used to study the purine nucleotide metabolism in response to 2, 4, and 6 h of ischemia and to the same ischemia periods followed by 1 h of reperfusion. All purine intermediates from ATP to uric acid were determined in skeletal muscle with a high-performance liquid chromatography (HPLC) system. The major metabolic event during ischemia is to temporarily save the nucleotide pool as inosine-5'-monophosphate (IMP. On restitution of the circulation as the energy state recovers, the IMP is converted back to AMP via the purine nucleotide cycle. Six hours of ischemia is associated with irreversible damage and no recovery fo the adenine nucleotides on reperfusion. Fast-twitch muscles appear to be more susceptible than slow-twitch muscles in response to ischemia and reperfusion. A severalfold increase of intracellular hypoxanthine occurred during ischemia, whereas uric acid formation is observed only after reperfusion. These findings are discussed in relation to the proposed role of xanthine oxidase, as an enzyme generating tissue-injurious oxygen free radicals.
 ...
PMID:Purine metabolism after in vivo ischemia and reperfusion in rat skeletal muscle. 236 Jun 63

Inherited adenine phosphoribosyltransferase (APRT) has a recessive transmission. When it is very important, adenine can't be restored into nucleic acids pool and will changed into 2,8-dihydroxyadenine (2,8-DHA) by xanthine oxidase. To date in all countries but Japan, 2,8-DHA urolithiasis is observed only into homozygotic subjects with complete APRT deficiency Commonly, its onset is observed in childhood often dramatically. The authors report two new pediatric cases into new french families. First a 8 years old boy with spontaneous elimination of two lithiasis after right lumbar pain. Secondly an infant (nineteen months) who has presented an acute renal failure with anuria. Bilateral lithiasis included into pyelourectal junctions have been pulled out by bilateral surgical pyelotomy. In each case, lithiasis were radiolucent and diagnosis made by ultrasonography. The uric acid metabolism was normal and it is the infra red spectrophotometric study of stones that had recognised the 2,8-DHA component. In the second case, bilateral residual lithiasis have been broken by piezoelectric extra-corporeal lithotripsy with good tolerance and favorable result. The two children received preventive treatment. After 36 and 19 months they have no recurrence. In the literature, the frequency of 2,8-DHA lithiasis is very more low than the theoretical of homozygotics in population (1/100,000). The common confusion with uric lithiasis is one possible explanation. So spectrophotometric study of radiolucent stones was meant to be realised when uric metabolism is not disturbed.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:[2,8-dihydroxyadenine lithiasis. 2 new pediatric cases of an unknown metabolic deficit. The use of extracorporal lithotripsy]. 238

Complete cessation of flow in isolated rat hearts for 90 min resulted in a gradual breakdown of ATP and concomitant accumulation of degradation products, such as adenosine, inosine (major break-down product), hypoxanthine, and, to a lesser extent, xanthine. After 45 min of ischemia, the content and relative composition of purines hardly changed, whereas the AMP content continued to rise. This finding points to constraints on AMP degradation and flux through the degradation pathway from adenosine to uric acid in the ischemic heart. In myocardial preparations, the cells of which were deliberately disrupted by freezing and thawing before anoxic incubation, AMP did not accumulate and was finally converted to hypoxanthine. These results indicate that compartmentalization of substrates and enzymes is responsible for the observed preferential accumulation of AMP and inosine in the ischemic heart. Inhibition of hypoxanthine degradation is explained by the absence of oxygen. Restoration of flow and oxygen supply abolished the inhibition of metabolic flux. Accumulated purines were released into the coronary effluent and, concomitantly, further metabolized. Comparison of tissue levels of hypoxanthine, xanthine, and uric acid before reperfusion and the amounts released during reperfusion indicates that in rat myocardium substantial amounts of potentially hazardous xanthine oxidase-derived reactive oxygen species are likely to be formed during the early reperfusion phase.
 ...
PMID:Degradation of adenine nucleotides in ischemic and reperfused rat heart. 278 5

Since only little xanthine oxidase (XO) activity in mammalian brain was detected in earlier reports, the major end product of AMP degradation in the brain has been believed to be hypoxanthine. Our recent experimental study however, has indicated the presence of uric acid in the rat brain subjected to focal ischemia or cold injury. Allopurinol, a xanthine oxidoreductase inhibitor, has been found to markedly suppress the uric acid production in the same experimental settings. These results suggested that uric acid is generated from hypoxanthine by enzymatic reaction in injured brain tissue. The aim of this experiment is to prove the existence of xanthine oxidoreductase activity in brain tissue. Xanthine oxidoreductase activity in rat cerebral tissue was measured immediately or at 24-hour after decapitation. Under pentobarbital anesthesia, twenty Sprague-Dawley rats were killed by decapitation following washout of the blood by trans-cardiac perfusion with cold physiological saline. Immediately or after 24 hours of decapitation ischemia, the forebrain was removed and homogenized in 6 ml ice cold 0.05 M potassium phosphate buffer (pH 7.8) containing 1 mM phenylmethylsulfonyl fluoride, 0.3 mM EGTA, and 10 mM dithiothreitol. The homogenate was centrifuged at 100,000 g for 60 min and then the supernatant was dialyzed overnight against 0.05 M potassium phosphate buffer (pH 7.8). Aliquot of each dialyzed supernatant (sample) and standard xanthine solution with NAD was reacted at 37 degrees C for 15 min to measure the combined activity of xanthine dehydrogenase (XDH) and XO. For the measurement of XO, standard xanthine solution without NAD was used.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:[Xanthine oxidoreductase activity in rat brain tissue: the changes after decapitation]. 280 24

Our recent studies have indicated that release of ATP/ADP from platelets causes enhanced O2-. responses in stimulated neutrophils. The current investigations were designed to provide further details of this phenomenon, to determine the structure-function correlates of the adenine compounds, and to assess if the results might be explained by the formation of a single metabolic product of ATP. ATP, ADP, AMP and adenosine enhanced O2-. responses of rat neutrophils stimulated with immune complexes or formyl chemotactic peptide (FMLP) but had no effect on responses of phorbol ester-stimulated neutrophils. Similar results were obtained in human neutrophils stimulated with immune complexes; when FMLP was the agonist, the results were divergent: ATP and ADP enhanced the responses, whereas AMP and adenosine were inhibitory. In structure-function studies, hydrolytically resistant forms of ATP (and other adenine nucleotides) containing blocked or cross-linked phosphate groups were active, suggesting that hydrolysis of these compounds to a common metabolic product is not required for their effects on O2-. responses. In contrast, other chemical modifications of the ribose ring or adenine base of ATP resulted in greatly diminished activity. To further pursue the question of whether metabolism of the adenine compounds via the adenosine pathway was related to the observed effects on O2-. responses, addition to rat neutrophils of inhibitors of adenosine deaminase, S-adenosyl homocysteine hydrolase, or xanthine oxidase failed to reproduce or augment the enhancement effects of the adenine compounds on O2-. responses, suggesting that metabolism of the adenine compounds to a common product may not be a requirement for the observed effects. Although the manner by which the adenine compounds affect O2-. responses is not known, the data suggest that adenosine and adenine nucleotides have important regulatory effects on oxygen radical responses of stimulated neutrophils.
 ...
PMID:Regulatory effects of adenosine and adenine nucleotides on oxygen radical responses of neutrophils. 283 59

Using density gradient centrifugation, human trophoblastic cells were enriched from mixed cell populations of enzymatically dispersed first- and third-trimester placentae. Over 95 per cent of the cells recovered were of epithelial (i.e., trophoblastic) origin, as evidenced by their cytokeratin intermediate filament positivity and vimentin negativity, examined using indirect immunofluorescence, and also by their high content of human chorionic gonadotrophin. The activities of key enzymes involved in purine degradation and re-utilization (5'-nucleotidase; AMP-deaminase; hypoxanthine phosphoribosyltransferase (HPRT); xanthine dehydrogenase/oxidase) as well as the total activity of alkaline phosphatase were measured in the trophoblastic cells. A six-fold increase in the trophoblastic alkaline phosphatase activity was noted between the first and third trimester. A 40 per cent decrease was noted in the activity of 5'-nucleotidase, which, on the basis of kinetic properties, appears to have a dominant role in the dephosphorylation of placental nucleoside-5'-monophosphates. The trophoblastic activities of AMP-deaminase, HPRT, and xanthine dehydrogenase/oxidase did not change as a function of the gestational age. In view of the relative activities of the latter two enzymes, hypoxanthine formed in the trophoblast appears more likely to be re-utilized than degraded to uric acid.
 ...
PMID:Activities of key enzymes of purine degradation and re-utilization in human trophoblastic cells. 283 9

The enzymatic inosine 5'-monophosphate assay described by Grassl [in, Methods of Enzymatic Analysis (H. U. Bergman, ed.), pp. 2168-2171, Academic Press, New York (1974)] is highly nonspecific, as ITP, ATP, ADP, AMP, and adenosine react stoichiometrically. The reactivity with the adenine derivatives is due to the tri- and diphosphatase activity of alkaline phosphatase (AP), coupled with adenosine deaminase (and possibly AMP deaminase) contamination of commercially available preparations of AP, purine-nucleoside phosphorylase, and/or xanthine oxidase. The inclusion of coformycin (0.05 microgram/ml), a potent inhibitor of these deaminases, completely eliminated the cross-reactivity. ITP, however, still reacted stoichiometrically due to the tri- and diphosphatase activity of AP. Meyer and Terjung [Amer. J. Physiol. 237 C111-C118 (1979)] introduced a modification of Grassl's procedure, substituting 5'-nucleotidase for AP. It has been found that this disallows reactivity with ATP, ADP, and ITP but that AMP and adenosine still react completely. Coformycin prevents this cross-reactivity. It is therefore recommended that the assay be carried out with 5'-nucleotidase (instead of AP) and coformycin, in order to achieve a more specific assay, and one more suitable for use with whole tissue extracts.
 ...
PMID:An enzymatic inosine 5'-monophosphate assay of increased specificity. 298 81


<< Previous 1 2 3 4 5 6 7 8 Next >>