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PubMed1990

Metabolic alterations in burn patients: detection of adenosine triphosphate degradation products and lipid peroxides.

Seven patients admitted to the University of Michigan Burn Center with greater than 20 per cent total body surface area burns were studied for evidence of oxygen radical production, as demonstrated by serum lipid peroxides, and adenosine triphosphate (ATP) degradation, based upon ATP degradation products in blood (serum purines) and urine (urine purines and urine uric acid). Lipid peroxides (conjugated dienes) were elevated beginning on day 1 postburn and remained elevated up to day 5, the duration of the study. ATP degradation products were elevated during the initial 24 h postburn but rapidly fell to normal levels. This study provides evidence of biochemical alterations in thermally injured patients similar to observations in animal models which demonstrate that ATP degradation and the production of oxygen radicals are part of the initial response to thermal trauma.

Adenosine Triphosphate↗
PubMed1977

The effect of non-steroidal anti-inflammatory drugs on adenosine triphosphate content and histamine release from rat peritoneal cell suspensions rich in mast cells.

1 Non-steroidal anti-inflammatory drugs (NSAID) suppressed compound 48/80-induced histamine release from rat peritoneal cells in vitro in a dose-dependent manner. 2 NSAID suppressed the adenosine triphosphate (ATP) content of rat peritoneal cells in vitro and this correlated strongly with the suppression of compound 48/80-induced histamine release. 3 The correlation demonstrated suggests that the mechanism of action of NSAID in the rat peritoneal cells is via depletion of cellular ATP.

Adenosine Triphosphate↗
PubMed2006

Intracoronary adenosine triphosphate for refractory coronary artery spasm.

A 62-year-old woman underwent aortic valve replacement for aortic stenosis. Her hemodynamics deteriorated with ST-T depression 6 hours postoperatively. Emergency coronary catheterization showed diffuse right coronary artery spasm. The spasm persisted despite intracoronary infusion of nitrates and calcium antagonists. Intracoronary adenosine triphosphate infusion finally resolved the spasm and stabilized the cardiac function.

Adenosine Triphosphate↗
PubMed1975

Stereochemical course of the adenosine triphosphate phosphoribosyltransferase reaction in histidine biosynthesis.

The product of the first reaction in histidine biosynthesis is shown by optical rotation measurements on three derivatives to have inverted, beta stereochemistry at the newly formed bond. This is in contrast to alpha linkage expected on the basis of previously observed exchange, specificity, and covalent intermediate phenomena. The postulate double displacement mechanism for adenosine triphosphate phosphoribosyltransferase must be modified to account for the product stereochemistry.

Adenosine Triphosphate↗
PubMed1998

Adenosine triphosphate causes vasospasm of the rat femoral artery.

OBJECTIVE: Adenosine 5'-triphosphate (ATP) causes vasoconstriction by activation of P2-purinoceptors on vascular smooth muscle cells. Erythrocytes contain ATP at a concentration (1.6 mmol/L) that contracts smooth muscle. Previous studies of hemoglobin solutions did not assess whether the vasoactivity was caused by ATP rather than or in addition to hemoglobin. It was hypothesized that the hemolysis of erythrocytes that occurs after subarachnoid hemorrhage releases ATP in concentrations that cause vasospasm. METHODS: Thirty-eight rats were randomly assigned to undergo placement of one of the following compounds in a silastic elastomer cuff around each femoral artery: 1) agarose gel (n = 8); 2) dog erythrocyte hemolysate (n = 8); 3) purified human hemoglobin (Hemolink; Hemosol, Inc., Toronto, Canada; n = 8); 4) ATP (n = 8); or 5) clotted autologous blood (n = 6). The amounts of hemoglobins and adenine nucleotides in the compounds were measured by spectrophotometry and high pressure liquid chromatography. Hemolysate, purified hemoglobin, and ATP were mixed with agarose gel to create an artificial clot. Rats were killed and fixed by perfusion at physiological blood pressure 7 days after perivascular cuff and spasmogen placement. Vasospasm was assessed by image analysis of cross sections of fixed femoral arteries. Arteries were assessed for histopathological changes on 3-point scales. RESULTS: There was significant variance in arterial diameters among groups (mean diameter +/- standard deviation: agarose gel, 0.29 +/- 0.06; purified hemoglobin, 0.28 +/- 0.04; hemolysate, 0.24 +/- 0.05; ATP, 0.25 +/- 0.05; clotted blood, 0.24 +/- 0.01; P < 0.05, analysis of variance, n = 11-20). Animals exposed to clotted blood, hemolysate that contained ATP, or ATP, developed vasospasm, whereas purified hemoglobin and agarose did not cause vasospasm. Endothelial proliferation and perivascular inflammation were more severe (P < 0.05) in arteries exposed to clotted blood, purified hemoglobin, and hemolysate. CONCLUSION: These results suggest that ATP may be a vasospastic substance released by erythrocyte hemolysis. The concentration of ATP in impure solutions of hemoglobin is too low to account for the vasoactivity of these solutions. The discrepancy between arterial narrowing and histopathological changes suggests that either histopathological changes may not be an important correlate of arterial vasospasm or that other substances are important in vasospasm.

Adenine Nucleotides↗
PubMed2004

Adenosine triphosphate levels in steelhead (Oncorhynchus mykiss) eggs: an examination of turnover, localization and role.

The dynamics of energy production and utilization in fish eggs before and shortly after fertilization may be critical for embryo survival. Therefore, the current study examined the turnover of adenosine triphosphate (ATP) as well as examined the possible role and localization of ATP in unfertilized steelhead (Oncorhynchus mykiss) eggs and early embryos. The mean ATP level in unfertilized steelhead eggs was 1.92+/-0.10 (mean+/-S.E.M., n=17) nmol ATP per egg. Exposure of the unfertilized egg to 10 degrees C water (water activation) and fertilization resulted in comparable and substantial decreases (approx. 20-50%) in egg ATP levels within 3 min. This suggests that the energy expended at fertilization is used in response to water activation rather than fertilization per se. Unfertilized eggs maintained in ovarian fluid for 9 days at 10 degrees C under air showed a progressive decline of fertility that reached zero after 6 days. In contrast, no significant changes were seen in ATP levels throughout this 9 days period. Thus, fertility does not positively correlate with egg ATP levels in stored eggs. In the unfertilized egg, the ATP stored in the yolk accounted for approximately 1.5% of the total egg ATP. After fertilization, the concentration of ATP in the yolk increased approximately seven-fold, with the yolk and blastoderm each now accounting for approximately 20% of the total remaining ATP. Finally, to estimate the changes in oxidative metabolism following fertilization, the cyanide (KCN)-sensitive decline in total ATP was determined for unfertilized eggs and 1 day embryos. In the presence of KCN, ATP levels declined to approximately 50% within 24 h in both unfertilized eggs as well as embryos; the rates of ATP decline were not different. Therefore, there was not a discernible increase in ATP generation by oxidative phosphorylation at the time of fertilization.

Adenosine Triphosphate↗
PubMed1986

Adenosine triphosphate content of Mycobacterium leprae isolated from armadillo tissue by Percoll buoyant density centrifugation.

A buoyant density centrifugation procedure using Percoll was developed for the isolation and purification of Mycobacterium leprae from experimentally infected armadillo liver tissue. The method separates the bacteria from host adenosine triphosphate (ATP) and tissue debris and recovers 20-25% of the bacteria within 2-2 1/2 hours under controlled conditions. The mean ATP content (585 pg/10(6] of the purified bacteria was similar to cultivable bacteria. The organisms did not leak intracellular ATP when exposed to phosphate buffer. Temperature-dependent ATP synthesis was observed within minutes and could be inhibited by 2,4-dinitrophenol. Freeze-thawing M. leprae as purified suspensions in buffer damaged the organisms, resulting in decreased ATP levels and an accelerated loss of ATP upon incubation under defined conditions. In vitro treatment with the antileprosy drug clofazimine increased the rate of ATP decay directly proportional to drug concentration.

2,4-Dinitrophenol↗
PubMed2001

Extracellular Adenosine Triphosphate Triggers Arrhythmias and Elemental Redistribution in Electrically Stimulated Rat Cardiac Myocytes.

An increase in extracellular adenosine triphosphate (ATP) is arrhythmogenic in rat cardiac myocytes and extracellular ATP levels are elevated during cardiac ischemia. To gain insight into the mechanism by which the arrhythmic contractions are generated, we investigated changes in subcellular elemental content by electron probe microanalysis (EPMA) in isolated adult rat cardiac myocytes stimulated by the ATP analog, 2-methylthio-ATP (2-M-S-ATP). We also measured the effects of 2-M-S-ATP stimulation on myocyte cell shortening. In electrically stimulated myocytes, 2-M-S-ATP stimulation generated arrhythmic contractions and also increased the amplitude of cell shortening. However, only the arrhythmic contractions were reversed by 2-M-S-ATP washout. EPMA of freeze-dried cryosections of rapidly frozen 2-M-S-ATP-stimulated myocytes showed increased cytosolic Na and Cl, decreased K, but no significant change in mitochondrial Ca upon 2-M-S-ATP stimulation. The arrhythmias were abolished upon 2-M-S-ATP washout, and the observed changes in cytosolic elemental content also reversed upon agonist washout, thus suggesting that the increased Na and Cl, and decreased K, are specifically associated with the ATP-dependent spontaneous contractile activity. The observed increase in intracellular Na upon 2-M-S-ATP stimulation may explain our observation of prolonged relaxation time of 2-M-S-ATP-stimulated contractions. This may be due to inhibition of Ca(2+) efflux via the Na(+) Ca(2+) exchanger.

Journal Article↗
PubMed1999

Lack of squamous cell lung carcinoma in vitro chemosensitivity to various drug regimens in the adenosine triphosphate cell viability chemosensitivity assay.

A pilot study on squamous cell lung carcinoma (LC) chemosensitivity in adenosine triphosphate cell viability chemosensitivity assay (ATP-CVA) was performed. Besides the histological investigation, a modified ATP-CVA was used for the analysis of cancer cell chemosensitivity to four drug regimens, including topotecan, a promising agent for non-small-cell lung cancer (NSCLC) chemotherapy. Results of in vitro chemosensitivity testing showed chemoresistance or only weak response in the predominant amount of tumors.

Aged↗
PubMed1992

Adenosine triphosphate in semen and other sperm characteristics: their relevance for fertility prediction in men with normal sperm concentration. World Health Organization Task Force on the Prevention and Management of Infertility.

OBJECTIVE: To evaluate the power of sperm characteristics and of the semen content of adenosine triphosphate (ATP) in predicting the occurrence of pregnancy in infertile couples. DESIGN: This is a prospective study monitoring the occurrence of pregnancy during 400 days of follow-up. SETTINGS: Couples were recruited in 10 centers, and data were analyzed at the World Health Organization Headquarters. PATIENTS: Of 361 couples recruited, 306 satisfied the following criteria: infertility of at least 12 months' duration, anatomically normal female ovulating regularly, sperm concentration greater than 20 x 10(6)/mL, valid semen data, and ATP available before conception. INTERVENTIONS: None. MAIN OUTCOME MEASURE: The occurrence of pregnancy. RESULTS: Ninety-six couples (31.4%) achieved conception. Duration of infertility less than 3 years was associated with higher conception rate (41.1%) than longer duration (28.2%). None of the semen characteristics nor the ATP content predicted the occurrence of pregnancy. CONCLUSIONS: Neither conventional sperm characteristics nor semen ATP can predict the occurrence of pregnancy among couples in which the female partner is normal and the male partner has sperm concentration greater than 20 x 10(6)/mL.

Adenosine Triphosphate↗
PubMed1981

Increase of acetylcholine-receptor sensitivity by adenosine triphosphate: a novel action of ATP on ACh-sensitivity.

1. The sensitivity of the nicotinic acetylcholine (ACh)-receptor, measured as the amplitude of ACh-current induced by iontophoretic application of ACh to the frog skeletal muscle endplate, was increased by the action of adenosine triphosphate (ATP). 2. This potentiation was not due to the effect of ATP on ACh-esterase, since the increase of the sensitivity could also be demonstrated by use of carbachol (CCh). 3. Kinetic analysis of the effect of ATP on the dose-response curve of CCh-current suggests that ATP increases the ACh-sensitivity by acting on the allosteric site of receptor-ionic channel complex without changing the affinity of ACh for its recognition site. 4. The equilibrium potential and the life-time of the endplate current (e.p.c.) are not altered by the presence of ATP. 5. These results suggest that ATP increases the ACh-sensitivity by increasing either the conductance of unit channels or the total number of available channels.

Acetylcholine↗
PubMedDate not supplied

The effect of dextran-40 on platelet adenosine triphosphate release in vitro.

Studies of dextran's effect on platelet function have revealed inconclusive results; some reports have suggested it acts as an aggregating agent, others as an inhibitor to aggregation. This study demonstrates the inhibitory effect of dextran (40,000 MW) on in vitro platelet adenosine triphosphate (ATP) release when stimulated by conventional aggregatory reagents. These data support inhibition of platelet surface phenomena, possibly involving receptor sites, rather than intracellular phenomena as the mechanism of dextran's anti-aggregatory effect. Significant inhibition occurs in vitro at dextran levels approximately twice that normally attained in vivo.

Adenosine Triphosphate↗
PubMed1979

Relaxation of guinea-pig fundic strip by adenosine, adenosine triphosphate and electrical stimulation: lack of antagonism by theophylline or ATP treatment.

1 Theophylline relaxed isolated strips of guinea-pig stomach fundus in a dose-dependent manner; above 50 to 100 microM responses showed no fade for up to 90 min. 2 Relaxant responses to adenosine, adenosine triphosphate (ATP), noradrenaline, and to electric field stimulation of non-adrenergic inhibitory nerves were not affected in a significant manner in the presence of 50 microM theophylline. 3 In tissues which showed complete fade of initial responses in the continued presence of 50 microM ATP, the effects of stimulation of non-adrenergic inhibitory nerves remained unaltered, suggesting that the ATP receptor has no function in non-adrenergic inhibitory transmission in this tissue. 4 These findings are opposite to those of Okwuasaba, Hamilton & Cook (1977), who claimed that 50 microM theophylline almost fully inhibited relaxation induced by adenosine ATP and nerve stimulation and that ATP-induced fade also abolished sensitivity to inhibitory nerve stimulation.

Adenosine↗
PubMed2006

Altered creatine kinase adenosine triphosphate kinetics in failing hypertrophied human myocardium.

BACKGROUND: The progression of pressure-overload left ventricular hypertrophy (LVH) to chronic heart failure (CHF) may involve a relative deficit in energy supply and/or delivery. METHODS AND RESULTS: We measured myocardial creatine kinase (CK) metabolite concentrations and adenosine triphosphate (ATP) synthesis through CK, the primary energy reserve of the heart, to test the hypothesis that ATP flux through CK is impaired in patients with LVH and CHF. Myocardial ATP levels were normal, but creatine phosphate levels were 35% lower in LVH patients (n = 10) than in normal subjects (n = 14, P < 0.006). Left ventricular mass and CK metabolite levels in LVH were not different from those in patients with LVH and heart failure (LVH+CHF, n = 10); however, the myocardial CK pseudo first-order rate constant was normal in LVH (0.36 +/- 0.04 s(-1) in LVH versus 0.32 +/- 0.06 s(-1) in normal subjects) but halved in LVH+CHF (0.17 +/- 0.06 s(-1), P < 0.001). The net ATP flux through CK was significantly reduced by 30% in LVH (2.2 +/- 0.7 micromol x g(-1) x s(-1), P = 0.011) and by a dramatic 65% in LVH+CHF (1.1 +/- 0.4 micromol x g(-1) x s(-1), P < 0.001) compared with normal subjects (3.1 +/- 0.8 micromol x g(-1) x s(-1)). CONCLUSIONS: These first observations in human LVH demonstrate that it is not the relative or absolute CK metabolite pool sizes but rather the kinetics of ATP turnover through CK that distinguish failing from nonfailing hypertrophic hearts. Moreover, the deficit in ATP kinetics is similar in systolic and nonsystolic heart failure and is not related to the severity of hypertrophy but to the presence of CHF. Because CK temporally buffers ATP, these observations support the hypothesis that a deficit in myofibrillar energy delivery contributes to CHF pathophysiology in human LVH.

Adenosine Triphosphate↗
PubMed2003

Correlation between the physicochemical property of some nonsteroidal anti-inflammatory drugs and changes in adenosine triphosphate, glutathione and hemoglobin in rat erythrocytes.

This study was conducted to explore the relationship between physicochemical property and toxic effectiveness using rat red blood cells (RBCs). The toxic effectiveness of acid nonsteroidal anti-inflammatory drugs (NSAIDs) was systemically examined by the depletion of intracorpuscular adenosine triphosphate (ATP), glutathione (GSH), and hemoglobin (Hb) at various doses, increased every 5 fmol/RBC. When the RBCs were incubated with NSAIDs, the drugs attained maximum levels within RBC, and the levels were then reduced. The ATP depletion seemed to be observed on the excretion of the drugs prior to the depletions of GSH and Hb. The physicochemical properties of NSAIDs were obtained from QMPRPlus, SMILES code, and CS ChemRaw Ultra. Correlation between their physicochemical properties and their doses for the depletions of ATP, GSH and Hb was performed in comparison with those of the membrane bound enzyme (MBE) inhibiting- and methemoglobin (MHb)-generating drugs. The ATP depletion by NSAIDs was correlated with the GSH depletion and intracorpuscular levels of the drugs, but not with the Hb depletion. The GSH depletion was correlated with the Hb depletion and participated in the lipophilicity of the drugs.

Adenosine Triphosphate↗
PubMed1989

Relationship between cell adenosine triphosphate and glutathione content and protection by glycine against hypoxic proximal tubule cell injury.

We designed studies to characterize metabolic aspects of the protective effects of glycine and glutathione against hypoxic proximal tubule cell injury b clarifying the relationship between protection and preservation of tubule cell adenosine triphosphate (ATP) and glutathione levels. The tubule preparation was glutatione depleted as isolated although some recovery occurred during incubation at 37 degrees C, and this recovery was enhanced by treatment with glutatione precursors. Increasing the duration of hypoxia from 30 minutes to 60 minutes produced increasingly extensive lethal tubule cell injury that was almost completely prevented, even at the 60-minute duration, by inclusion of either 2 mmol/L glutathione or 2 mmol/L glycine in the tubule incubation medium. Cell ATP levels decreased to the same extent and at the same rate in protected and unprotected hypoxic tubules. Glycine- and glutathione-protected tubules maintained higher cell glutathione levels than unprotected tubules at all durations of hypoxia studied. However, completely eliminating this increment of glutathione with either the gamma-glutamylcysteine synthetase inhibitor, buthionine sulfoximine, or the glutathione reductase inhibitor, 1,3-bis(2-chloroethyl)-1-nitrosourea, did not prevent protection. The data indicate that the striking protection against hypoxic injury to the isolated tubules provided by treatment with glycine or glutathione is independent of preservation of tubule cell ATP and glutathione levels, to the extent that difference of these levels can be discriminated in intact cells with present methods.

Adenosine Triphosphate↗
PubMed2000

Adenosine triphosphate mobilizes cytosolic calcium and modulates ionic currents in mouse taste receptor cells.

By using photometry and the patch clamp technique, we identified P(2Y)-like receptors in mouse taste receptor cells (TRCs) and found them to be coupled to Ca(2+) mobilization and ionic current modulation. Particularly, adenosine triphosphate (ATP) and the P(2Y) agonist 2-methylthio-ATP increased intracellular Ca(2+) by stimulating the phosphoinositide pathway, whereas beta, gamma-methylene-D-ATP, a P(2X) agonist, was ineffective. In a distinctive TRC subpopulation, ATP closed Ca(2+) channels. This regulation may underlie the negative feedback tuning neurotransmitter release. By mobilizing intracellular Ca(2+), ATP activated Ca(2+)-dependent Cl(-) channels, the intracellular event that may universally occur upon taste stimulation triggering IP(3) formation and Ca(2+) release in the TRC cytoplasm.

Adenosine Triphosphate↗
PubMed1993

A 31P NMR spectroscopy study of Xenopus laevis heart perfused in vitro with creatinol-O-phosphate, phosphocreatine, adenosine triphosphate, fructose diphosphate and ouabain.

Xenopus laevis heart was studied by 31P NMR using a 200 MHz proton spectrometer; hearts were perfused, at pH 7.35 and room temperature, with normal oxygenated or K(+)-enriched Ringer. Solution was later added with creatinol-O-phosphate (COP), phosphocreatine (PCr), adenosine triphosphate (ATP), fructose-1,6-diphosphate (FDP) and ouabain. NMR spectra of the heart show organic phosphomono- and phosphodi-esters, inorganic phosphate, PCr, overlapping alpha-ATP/ADP and gamma-ATP/beta-ADP, and beta-ATP signals. Their chemical shift positions and areas showed no significant changes in the course of 1.5 h perfusions with either solution, except in a few preparations, whether the heart was beating or reversibly arrested. While COP reduced the signals in beating hearts, the same spectra exhibited no consistent, substantial changes under PCr, ATP and FDP 1 to 10 mM, pH 7.35 perfusion with either solution, nor when ouabain mumol was added. The spectra are briefly discussed in comparison with those observed in the perfused heart of mammals (mostly rat), and particularly with those obtained in the frog (Rana temporaria) heart, both by analysing the bioenergetic equilibria on the basis of total tissue substrate levels measured in extracts of freeze-clamped tissue, and by evaluating cytochrome-b, flavin and pyridine nucleotide in vitro oxido-reduction read-outs in separate, similar experimental settings.

Adenosine Triphosphate↗