Adenosine Triphosphate Diphosphate Research Articles

A novel assay of thrombotic risk

It is widely believed that platelet responsiveness can be used as a marker for assessing thrombotic risk in patients. Therefore, there have been many attempts to develop suitable assays for quantifying platelet responses in clinical samples 1. Platelet aggregometry is widely used, but is limited in its ability to assess platelet hyper-responsiveness. In order to develop a better assay of thrombotic risk, we use a novel assay to evaluate platelet secretion of adenosine triphosphate & diphosphate (ATP/ADP) in response to various agonists. This assay measures both the maximal amount of adenine nucleotides released by a range of platelet activators and the potency of each activator.

Energy Charge Is Not Decreased in Lymphocytes of Patients With Leber??s Hereditary Optic Neuropathy With the 11778 Mutation

A defect in mitochondrial energy conservation is strongly suggested to be involved in the pathogenesis of Leber's hereditary optic neuropathy (LHON). The authors therefore compared the energy charge in lymphocytes among patients with LHON, their asymptomatic maternal lineages, and normal control subjects. Blood samples were obtained from 7 patients, 10 asymptomatic maternal relatives, and 16 normal subjects. Molecular analysis confirmed that all had the homoplasmic 11,778 point mutation in the mtDNA of their blood cells. The concentrations of adenosine triphosphate (ATP), diphosphate (ADP), and monophosphate (AMP) were determined by high-performance liquid chromatography. The energy charge was calculated as (ATP + 1/2 ADP)/(ATP + ADP + AMP). The mean energy charges of lymphocytes were 0.871 +/- 0.049 in patients with LHON, 0.884 +/- 0.061 in their asymptomatic maternal relatives, and 0.885 +/- 0.061 in normal controls, respectively. No statistically significant difference was found among the three groups. Although the study did not find the anticipated change in energy charge in peripheral blood cells, this neither confirms nor rejects the notion that a defect in the mitochondrial oxidative phosphorylation system is involved in the pathogenesis of LHON.

A spectrophotometric study of the interaction of VO 2+ with adenine in nucleotides

The interaction of VO 2+ with adenosine-triphosphate (ATP), -diphosphate (ADP), and -mono- phosphate (AMP) has been studied as a function of pH by differential UV-absorption spectroscopy. It could be demonstrated that at pH > 3 an interaction of the cation with the adenine ring takes place in the case of the VO/ATP and VO/ADP systems. At pH ⪯ 3 the metal-to-ligand interaction occurs only through the phosphate moieties of the nucleotides; this is also the behavior observed for the VO/AMP system, even at higher pH values. Results for the VO 2+/P 2O 7 4− and VO 2+/D-Ribose interactions are also presented.

Improved functional recovery of ischemic myocardium by suppression of adenosine catabolism

Isolated working rat heart preparations were used to ascertain whether the addition of adenosine and prevention of its catabolism could aid in the functional recovery of hearts following global ischemia. Hearts were infused with either 80 micro M EHNA (an adenosine deaminase inhibitor) or 20 micro M adenosine and EHNA in either normal (2.4 mM) or low (0.05 mM) calcium-containing buffer prior to clamping of the aorta for 30 minutes. In one series of hearts, postischemic concentrations (mumoles/gram wet weight) of adenosine triphosphate (ATP), diphosphate (ADP), and monophosphate (AMP), adenosine, inosine, and hypoxanthine were measured; in another series, the recovery of aortic flow rate was used as a measure of functional recovery of ventricular muscle. With normal electrolyte balance, EHNA was unable to protect hearts against ATP loss and ventricular failure. Hearts with EHNA + adenosine recovered 14% of preischemic aortic output and ATP levels were slightly elevated at 0.93 mumole/gm. Those treated with either EHNA or EHNA + adenosine in low-calcium buffer recoverd 100% of their original aortic output. However, EHNA + adenosine maintained considerably higher ATP levels (1.57 mumoles/gm) than did EHNA alone (1.14 mumoles/gm) and was associated with faster initial recovery of aortic output. Thus the prevention of adenosine catabolism was insufficient for adequate ventricular recovery unless the tissue ATP was maintained above about 1.0 mumole/gm. EHNA + adenosine in a 0.05 mM Ca++ infusion solution conserved ATP, markedly improved the functional recovery of hearts, and thus may have a role to play in myocardial preservation during elective cardiac arrest.

Effects of transitory maternal pteroylglutamic acid (PGA) deficiency on levels of adenosine phosphates in developing rat embryos.

AbstractA transient maternal folic acid deficiency resulted in alterations in the concentrations of adenosine triphosphate (ATP), diphosphate (ADP), and monophosphate (AMP) in developing rat embryos. At the end of the treatment period the ATP level was markedly reduced and the pool of adenine (as ATP, ADP, and AMP) was decreased in experimental embryos. On the basis of these findings an explanation is suggested for the increased oxygen consumption previously observed for rat embryos from folic acid‐deficient females.

The effects of phenobarbitone, leptazol, dexamphetamine, iproniazid, imipramine, LSD, chlorpromazine, reserpine and hydroxyzine on the in vivo levels of adenine nucleotides and phosphocreatine in the rat brain.

1. Enzymic and ion-exchange chromatographic analyses were used to measure adenosine triphosphate (ATP), diphosphate (ADP) and monophosphate (AMP) in brain extracts from rats treated with a wide range of centrally acting drugs. Phosphocreatine (PC) was assayed by the acid molybdate method.2. An anaesthetic dose of phenobarbitone caused an increase in brain levels of ATP and PC, and a reduction in ADP and AMP. A convulsant dose of leptazol gave rise to precisely opposite effects. Subanaesthetic (hypnotic) and subconvulsive doses of the two drugs, respectively, produced no alterations in brain nucleotide levels.3. Among the psychotropic drugs, dexamphetamine, LSD and hydroxyzine, at the doses used, caused no changes in brain levels of the adenine nucleotides. Iproniazid and imipramine caused slight increases in the ATP level and ATP / ADP ratio, respectively. Chlorpromazine failed to give rise to any effect in the nucleotides 3 hr after administration, but produced a rise in brain ATP after 6 hr. Reserpine, on the other hand, caused a fall in the ATP/ADP ratio 6 hr after injection.4. These results indicate that some psychotropic drugs can cause small changes in the rat brain ATP/ADP ratio but do not support claims by certain workers that such changes correlate closely with the behavioural effects of these drugs.