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PubMed1991

Enhanced restoration of adenine nucleotides in rat liver following extended preservation in UW solution by provision of adenosine during reperfusion.

The extensive reduction of adenine nucleotides during preservation coupled with the loss of salvageable precursors during initial reflow may exacerbate recovery of adenine nucleotides in allograft liver following transplantation. The objective of this study was to assess whether provision of adenosine during reperfusion of rat liver stored for 20 hr in University of Wisconsin solution could enhance adenine nucleotide restoration. ATP and total adenine nucleotide content of livers perfused with an oxygenated Krebs/fluorocarbon solution containing 1 mM adenosine were restored to levels in vivo within 30 min of perfusion. Adenine nucleotide recovery in livers perfused without adenosine was only 65% of normal. Acute nutritional deprivation of the donor rats had no effect on adenine nucleotide restoration. These results indicate that a conditional deficiency of intracellular nucleotide precursors exists during initial reperfusion of liver subjected to extended storage in UW solution. Provision of supplemental adenosine to the allograft liver during initial reflow appears warranted to promote full and rapid restoration of adenine nucleotide content following extended preservation ex vivo.

Adenine Nucleotides↗
PubMed1982

The in vitro effect of adenine on pyruvate kinase-deficient red cells.

In pyruvate kinase (PK)-deficient blood with high levels of reticulocytes, the degree of haemolysis after incubation at 37 degrees C for 48 h was halved by the inclusion of adenine in the medium. the decrease in haemolysis was associated with a higher ATP level but was not related to the pH of the incubation mixture. The incorporation of adenine into nucleotides studied over a 3 h period was similar in normal and PK-deficient blood. The observed increase in cellular ATP was equivalent to that shown by radioactive measurements to have been synthesized from added adenine. Inhibition of mitochondrial oxidative phosphorylation in the reticulocytes of the PK-deficient blood by KCN reduced the amount of adenine taken up by the cells by a factor of 3 and altered the pattern of incorporation into the nucleotides. Only 25% of the adenine which entered the blood cells was converted into ATP compared with 85% in the absence of cyanide. Despite the synthesis of small amounts of ATP from labelled adenine, the overall ATP content fell to less than 50% of its original level. It is suggested that incubation with adenine increased the ATP level in the reticulocytes by virtue of mitochondrial oxidative phosphorylation thereby reducing the haemolysis of these cells.

Adenine↗
PubMed1975

Studies on citrate-phosphate-dextrose (CPD) blood supplemented with adenine.

The effect of varying adenine concentrations in citrate-phosphate-dextrose (CPD) blood was studied in an attempt to optimize the storage conditions for human erythrocytes with regard to posttransfusion viability and oxygen release function. The maintenance of diphosphoglycerate (DPG) was impaired by adenine supplementation; this effect was closely related to the adenine concentration. A 0.25 mM adenine concentration in CPD blood improved the adenosine triphosphate (ATP) levels and the posttransfusion viability markedly, without appreciably impairing the DPG maintenance. The results suggest that CPD solution supplemented with adenine to give a 0.25 mM concentration in the blood is a better preservative for human erythrocytes than the commonly used acid-citrate-dextrose (ACD), CPD, and ACD-adenine solutions with regard to posttransfusion viability and oxygen release function. Adenine addition to this low concentration is not expected to cause renal damage even after massive transfusion.

Adenine↗
PubMed1976

Preparation and properties of 3-halopyridine--adenine dinucleotides, NAD+ analogues and model compounds.

The preparation of model compounds 1-(2',6'-dichlorobenzyl)-3-halogenopyridinium and the study of their properties were achieved. Their chemical reduction to the corresponding 1,4-dihydropyridines is proved by spectroscopic analysis. 3-Iodopyridine--adenine dinucleotide was prepared by enzymic transglycosidation while the 3-chloro, 3-bromo and 3-iodo pyridine--adenine dinucleotides were synthesized from 3-amino-pyridine--adenine dinucleotide. The 3-halogenopyridine--adenine dinucleotides were proved to be active as hydrogen acceptors with alcohol as a substrate. The absorption band at 290 nm of cinnamaldehyde appeared to be a very sensitive tool for studying the enzymic reaction. With the alcohol dehydrogenase from yeast, only slight activity was detected. 3-Halogenopyridine--adenine dinucleotides are competitive inhibitors with respect to nicotinamide--adenine dinucleotide with alcohol dehydrogenase from yeast, lactate dehydrogenase and malate dehydrogenase. The use of 3-iodopyridine--adenine dinucleotide as a heavy-atom derivative for X-ray structure determination is proposed.

Adenine Nucleotides↗
PubMed1986

Neuromodulation by adenine nucleotides, as indicated by experiments with inhibitors of nucleotide inactivation.

The adenine nucleotides AMP, ADP and ATP (3 X 10(-7) M and above) inhibited contractile responses to transmural nerve stimulation in guinea-pig ileum longitudinal muscle via a prejunctional action. Nucleotides assumed to inhibit the degradation of adenine nucleotides were employed to determine whether inhibition of contractile responses was elicited by adenine nucleotides per se, or required breakdown to adenosine. The IMP or 2'-deoxy AMP enhanced the prejunctional inhibitory effect elicited by AMP. A similar enhancement of the inhibitory effect of ADP and ATP was seen after administration of IDP and ITP, respectively. The inhibitory effect of adenosine was not enhanced by inosine, IMP or IDP. The 5'-nucleotidase inhibitor, TDP enhanced inhibition elicited by ADP. In contrast, alpha, beta-meADP did not influence the prejunctional inhibitory effect elicited by the adenine nucleotides. However, the combination of alpha, beta-meADP and IMP enhanced the inhibitory effect of ATP. The postjunctional contractile effect elicited by ADP and ATP was enhanced by pretreatment with inosine nucleotides, alpha, beta-meADP or TDP, indicating decreased inactivation of ADP and ATP during concurrent nucleotide administration. The fact that the prejunctional effect of adenine nucleotides can be enhanced by forms of pretreatment known to antagonize the breakdown of adenine nucleotides, constitutes strong evidence for prejunctional action per se by adenine nucleotides.

Adenine Nucleotides↗
PubMed2006

Naturally occurring adenines within mRNA coding sequences affect ribosome binding and expression in Escherichia coli.

Translation initiation requires the precise positioning of a ribosome at the start codon. The major signals of bacterial mRNA that direct the ribosome to a translational start site are the Shine-Dalgarno (SD) sequence within the untranslated leader and the start codon. Evidence for the presence of many non-SD-led genes in prokaryotes provides a motive for studying additional interactions between ribosomes and mRNA that contribute to translation initiation. A high incidence of adenines has been reported downstream of the start codon for many Escherichia coli genes, and addition of downstream adenine-rich sequences increases expression from several genes in E. coli. Here we describe site-directed mutagenesis of the E. coli aroL, pncB, and cysJ coding sequences that was used to assess the contribution of naturally occurring adenines to in vivo expression and in vitro ribosome binding from mRNAs with different SD-containing untranslated leaders. Base substitutions that decreased the downstream adenines by one or two nucleotides decreased expression significantly from aroL-, pncB-, and cysJ-lacZ fusions; mutations that increased downstream adenines by one or two nucleotides increased expression significantly from aroL- and cysJ-lacZ fusions. Using primer extension inhibition (toeprint) and filter binding assays to measure ribosome binding, the changes in in vivo expression correlated closely with changes in in vitro ribosome binding strength. Our data are consistent with a model in which downstream adenines influence expression through their effects on the mRNA-ribosome association rate and the amount of ternary complex formed. This work provides evidence that adenine-rich sequence motifs might serve as a general enhancer of E. coli translation.

Adenine↗
PubMed1977

Uptake and efflux of adenine and its derivatives in Neurospora crassa.

Conidia of wild-type Neurospora crassa, preincubated for 3 1/2 h in growth medium, showed a typical triphasic pattern of adenine uptake. The three phases consisted of a quick initial uptake, followed by a plateau phase, and then by a resume lowered uptake. A study of the relative influx and efflux of [14C] adenine showed that the plateau phase in fact is a period of transmembrane movement of adenine and adenine metabolites. The efflux during the plateau phase essentially cancelled out all the influx during the same period. The uptake curve derived after taking into account the effluxed portion of radioactivity indicated that the second phase represents a period of lowered uptake activity. The beginning of the lowered uptake activity during the second phase is correlated with the presence of a high intracellular level of ATP derived from exogenous [14C]adenine. At the end of the secod phase, the intracellular level of ATP is much smaller and the rate of adenine uptake increases again. Analysis of the acid-soluble pool after feeding [14C]adenine indicated the presence of other 14C-nucleotides, but no detectable levels of bases and nucleosides were present. However, chromatographic analysis of the medium indicated that efflux results essentially in the accumulation of bases. The significance of this finding in relation to efflux is discussed.

Adenine↗
PubMed1987

Regulation of mitochondrial adenine nucleotide content in newborn rabbit liver.

This study examined the relationship between postnatal metabolic and hormonal changes and the accompanying rapid increase in mitochondrial adenine nucleotide content (ATP + ADP + AMP) in rabbit liver. The cytosolic NAD+/NADH concentration ratio, calculated from tissue pyruvate and lactate values, increased linearly 6.6-fold during the 1st postnatal h. The mitochondrial NAD+/NADH concentration ratio, calculated from tissue acetoacetate and beta-hydroxybutyrate values, increased 28-fold by 30 min postnatal. These changes in NAD+/NADH suggest that tissue oxygenation occurs rapidly and that oxygen supply rather than substrate supply is limiting for mitochondrial respiration in the immediate postnatal period. The normal increase in mitochondrial adenine nucleotide content that occurs within 2 h after birth was inhibited by hypoxia (5% O2). Glucagon stimulated the postnatal increase in mitochondrial adenine nucleotides but had no effect in combination with hypoxia. Both glucose and somatostatin injections inhibited the increase in mitochondrial adenine nucleotides and increased the insulin-to-glucagon ratio. Isoproterenol or dibutyryl cAMP stimulated, but propranolol did not inhibit, the normal increase in mitochondrial adenine nucleotide content. Phentolamine did not stimulate the postnatal accumulation of adenine nucleotides. In summary, the results show that the insulin-to-glucagon ratio is probably the most important hormone regulator of the rapid recompartmentation of adenine nucleotides into the mitochondrial matrix and that tissue oxygenation is strictly permissive for this hormone effect in the first 2 h after birth.

3-Hydroxybutyric Acid↗
PubMed1981

Intramitochondrial adenine nucleotides and energy-linked functions of heart mitochondria.

Isolated rabbit heart mitochondria were incubated with varying amounts of inorganic pyrophosphate in 250 mM sucrose to specifically decrease the pool size of endogenous adenine nucleotides. The endogenous adenine nucleotide content decreased by as much as 80% as a result of this treatment. Phosphorylating respiration (state 3) declined from about 340 to 180 nAtoms O . min-1 . mg protein-1 over the full range of intramitochondrial adenine nucleotides measured (approx 7.5-1.5 nmol/mg protein). Uncoupled and nonphosphorylating (state 4) rates of respiration were not greatly affected by adenine nucleotide depletion. Respiratory activity of the adenine nucleotide-depleted mitochondria was enhanced by addition of exogenous adenosine 5'-triphosphate (ATP). Partial depletion (approx 40%) of the intramitochondrial adenine nucleotides resulted in an impaired ability of heart mitochondria to retain Ca2+. Premature Ca2+ efflux was associated with organelle swelling and altered energy coupling. Exogenous ATP or adenosine 5'-diphosphate (ADP) added prior to Ca2+ efflux restored Ca2+ retention in these mitochondria. Atractyloside inhibited the restoration of Ca2+ retention. This study indicates a significant role for endogenous adenine nucleotides in maintaining oxidative phosphorylation and Ca2+ transport in heart mitochondria. The results are discussed with regard to significance in ischemic heart damage.

Adenine Nucleotides↗
PubMed1975

Adenine nucleotides in the secretory granule fraction of rat islets.

Concomitant with glucose-induced insulin release, there occurred an increase of ATP from 4.40 plus or minus 0.21 to 23.16 plus or minus 0.52 pmol/100 islets/min (P less than 0.001) in the effluent from perifused rat islets. There is a linear relationship between circulating ATP and insulin levels both in the stimulated and basal state (r = 0.689, P less than 0.01). Islets incubated with labeled adenine for a short period of time (37.5 min) showed no release of radioactivity upon subsequent glucose-induced insulin release. Islets incubated for a prolonged interval with labeled adenine (150 min) showed an increase in acid soluble radioactivity in the effluent during glucose-induced insulin release. Following incubation of the islets with labeled adenine for 150 min, approximately 5% of the homogenate radioactivity was found in the secretory granules. Using column chromatography to separate the adenine nucleotides, the distribution of radioactivity among the various nucleotides in the secretory granule fraction was found to be: AMP 54.42 plus or minus 4.96%, ADP 14.20 plus or minus 1.63%, ATP 15.39 plus or minus 3.84%, and cAMP 16.07 plus or minus 2.11%. The distribution of radioactivity in the effluent adenine nucleotides after glucose-induced insulin release was: AMP 32.83 plus or minus 4.62%, ADP 24.52 plus or minus 2.77%, ATP 28.13 plus or minus 5.45%, and cAMP 26.01 plus or minus 3.34%. The absolute levels of adenine nucleotides in the secretory granules were ATP 4.19 plus or minus 0.88, ATP madp 7.94 plus or minus 2.20 and cAMP 4.46 plus or minus 1.74 pmol/ug prot. The levels in the islet effluent were ATP, 15.30 plus or minus 2.70, ATP qDP, 29.43 plus or minus 3.49 and cAMP 7.66 plus or minus 1.93 pmol/100 islets/min for the first ten min of glucose-stimulated insulin release. Thereafter there was a rapid decline in effluent cAMP while ATP and ADP remained in essentially equivalent amounts. The distribution of radioactivity and absolute levels of the adenine nucleotides in the effluent reflects that found in the secretory granules, confirming previous observations that insulin release is occurring by exocytosis.

Adenine Nucleotides↗
PubMed1987

Distinct effects of adenine and guanine starvation on DNA synthesis associated with different pool sizes of nucleotide precursors.

Guanine nucleotide depletion primarily causes a drastic inhibition of DNA synthesis, while adenine nucleotide depletion interferes with other vital functions before inhibiting DNA synthesis (M. B. Cohen and W. Sadée, Cancer Res., 43: 1589-1591, 1983). This study addresses the hypothesis that the presence of a large adenine nucleotide pool with direct access to DNA synthesis prevents immediate cessation of DNA synthesis under conditions of adenine starvation, while the small guanine-DNA precursor pool is readily exhausted under guanine starvation. Adenine, guanine, and deoxyadenosine tracers were incubated with asynchronized or synchronized S-49 cells, and tracer progression into cellular nucleotide pools and nucleic acids was measured. Compartmentation of the dATP pool into a functional DNA precursor pool and a general cellular pool could not be demonstrated with [3H]dAdo tracer experiments with S-phase cells. While guanine tracer was incorporated into DNA without delay (less than 5 min), consistent with a small functional guanine-DNA precursor pool, adenine tracer incorporation into DNA was associated with a substantial delay period (approximately 30 min) indicative of a large functional adenine-DNA precursor pool. These results suggest that the different size of the functional nucleotide precursor pools with rapid access to DNA synthesis accounts for the dramatic difference in the effects of purine antimetabolites that cause either adenine or guanine starvation.

Adenine↗
PubMed1987

Degradation and resynthesis of adenine nucleotides in adult rat heart myocytes.

The degradation and short-term resynthesis of adenine nucleotides have been examined in a preparation of isolated rat heart myocytes. These myocyte preparations are essentially free of vascular and endothelial cells, contain levels of adenine nucleotides quite comparable to those of intact heart tissue, and retain these components remarkably well for up to 2 h of aerobic incubation in the presence of 1 mM Ca2+. When the cells are rapidly and synchronously de-energized by addition of uncoupler, an inhibitor of respiration and iodoacetate, cellular ATP is degraded almost quantitatively to AMP. The AMP is then converted to either intracellular adenosine, which accumulates to high concentrations before release to the cell exterior, or to IMP. The relative contribution of these two pathways depends on the metabolic state of the cells just prior to de-energization, with IMP production favored when respiring cells are de-energized and adenosine formation predominant when glycolyzing myocytes are subjected to this treatment. Cells de-energized by anaerobiosis in the absence of glucose lose ATP and adenine nucleotides with the production of IMP and adenosine. Upon reoxygenation, these cells restore a high adenylate energy charge and about 60% of control levels of GTP. There is a net resynthesis of 5-7 nmol of adenine nucleotides.mg-1 protein with a corresponding decline in IMP. Added [14C]adenosine labels the adenine nucleotide pool, but little net resynthesis of adenine nucleotides via adenosine kinase can be detected. It therefore appears that a rapid regeneration of adenine nucleotides can occur via the enzymes of the purine nucleotide cycle in heart myocytes and is limited by the size of the IMP pool retained.

Adenine Nucleotides↗
PubMed1978

Cytotoxic and metabolic effects of adenosine and adenine on human lymphoblasts.

The metabolic and growth inhibitory effects of adenosine toward the human lymphoblast line WI-L2 were potentiated by the adenosine deaminase inhibitors erythro-9-(2-hydroxy-3-nonyl) adenine (EHNA) and coformycin. EHNA, 5 micron, or coformycin, 3.5 micron, at concentrations that inhibited adenosine deaminase activity more than 90% had little effect on cell growth or the metabolic parameters studied. Adenosine, 50 micron, plus EHNA, 5 micron, arrested cell growth in both parent and adenosine kinase-deficient lymphoblasts, implicating the nucleoside as the mediator of the cytostatic effect. Adenosine, 50 micron, in combination with the adenosine deaminase inhibitors reduced 14CO2 generation from [1-14C]glucose by 38%, depleted 5-phosphoribosyl-1-pyrophosphate by more than 90%, and reduced pyrimidine ribonucleotide concentrations. Uridine, 10 or 100 micron, reversed adenosine plus EHNA growth inhibition in WI-L2 but not in adenosine kinase mutants. Adenine, 500 micron, which may be converted to the same intracellular nucleotides as adenosine, reduced the growth rate by 50% in both parent and adenine phosphoribosyltransferase-deficient lymphoblasts. Although adenine also depleted cells of 5-phosphoribosyl-1-pyrophosphate and reduced pyrimidine ribonucleotide by 50%, the mechanisms of adenine and adenosine toxicity differ. In contrast to the ability of uridine to reverse adenosine cytostasis, growth inhibition by adenine was not reversed by uridine, indicating that pyrimidine ribonucleotide depletion is not the primary mechanisms of adenine toxicity.

Adenine↗
PubMed1978

Reversal of adenine-induced depression of mouse locomotor activity by amphetamine.

Adenine (200 mg/kg) was found to depress locomotor activity in mice. Dl-, and d-amphetamine reversed the depression of locomotor activity produced by adenine while l-amphetamine was found to be incapable of reversing the adenine-induced depression. The stimulation of mouse locomotor activity caused by dl- and d-amphetamine in mice treated with adenine was less than that caused by equal dosage of these agents in mice not treated with adenine. Mice treated with adenine showed marked depletion of brain norepinephrine, dopamine and serotonin, irrespective of whether or not they had been treated with d- or l-amphetamine, and whether or not these agents were capable of reversing adenine-induced depression of locomotor activity.

Adenine↗
PubMed1992

Metabolic consequences of adenine-phosphoribosyl transferase deficiency in V79 hamster fibroblasts.

Two APRT- clones (V79-E3 and V79-E1A) were isolated from V79 hamster fibroblasts treated with ethyl methanesulfonate. Selection involved sequential exposure of the mutagenized cells to the adenine analogues 8-azaadenine and 2,6-diaminopurine. To examine the influence of APRT deficiency on cell metabolism we determined the size and turnover of adenine ribonucleotide pools, the deoxyribonucleoside triphosphate pools, the rate of DNA synthesis, and the length of the cell cycle. Clone V79-E3 was hemizygous for aprt and carried a new chromosome, 3p-. Clone V79-E1A was quasi-tetraploid with a cell volume more than twice that of the WT cells. When the difference in size was taken into account, both clones behaved similarly. While WT V79 cells released no adenine into the medium, they excreted adenine at a rate of 6 pmol/min. This did not affect the size of the ATP pool. The main change in the deoxynucleotide pools was a marked decrease of the concentration of dCTP. The rate of DNA synthesis was the same in WT cells and in the diploid V79-E3 clone. APRT is known to recycle adenine produced during polyamine synthesis, but the enzyme apparently contributes little to the maintenance of adenine ribonucleotide pools of V79 fibroblasts.

Adenine↗
PubMed1990

Pharmacological activity of adenine dinucleotides in the periphery: possible receptor classes and transmitter function.

1. The pharmacological actions of adenine dinucleotides, in particular beta-nicotinamide adenine dinucleotide (NAD), beta-nicotinamide adenine dinucleotide phosphate (NADP) and a homologous series of alpha,omega-adenine dinucleotide polyphosphates has been reviewed. 2. It is apparent that many actions of NAD can be explained in terms of activation of P1-purinoceptors, but actions of NADP cannot be explained in terms of activation of P1- or P2-purinoceptors. 3. Similarly, pharmacological activities of P1,P3-diadenosine triphosphate and P1,P4-diadenosine tetraphosphate are not in keeping with activation of P1- or P2-purinoceptors. 4. In the vas deferens and urinary bladder, P1,P4-diadenosine tetraphosphate, P1,P5-diadenosine pentaphosphate and P1,P6-diadenosine hexaphosphate act on P2x-purinoceptors and can cause desensitization of these receptors. 5. It is suggested that classes of receptors for adenine dinucleotides exist which are distinct from either P1- or P2-purinoceptors. 6. It is also suggested that in view of the finding of high concentrations of alpha,omega-adenine dinucleotide polyphosphates in adrenal medullary chromaffin cells, and of the involvement of the P2x-purinoceptor in the vas deferens and urinary bladder with purinergic neuromuscular transmission, that alpha,omega-adenine dinucleotide polyphosphates may yet be discovered in autonomic neurones and serve as neurotransmitters.

Adenosine Diphosphate↗
PubMed2003

Sub-families of alpha/beta barrel enzymes: a new adenine deaminase family.

No gene coding for an adenine deaminase has been described in eukaryotes. However, physiological and genetical evidence indicates that adenine deaminases are present in the ascomycetes. We have cloned and characterised the genes coding for the adenine deaminases of Aspergillus nidulans, Saccharomyces cerevisiae and Schizosaccharomyces pombe. The A.nidulans gene was expressed in Escherichia coli and the purified enzyme shows adenine but not adenosine deaminase activity. The open reading frames coded by the three genes are very similar and obviously related to the bacterial and eukaryotic adenosine deaminases rather than to the bacterial adenine deaminases. The latter are related to allantoinases, ureases and dihydroorotases. The fungal adenine deaminases and the homologous adenosine deaminases differ in a number of residues, some of these being clearly involved in substrate specificity. Other prokaryotic enzymes in the database, while clearly related to the above, do not fit into either sub-class, and may even have a different specificity. These results imply that adenine deaminases have appeared twice in the course of evolution, from different ancestral enzymes constructed both around the alpha/beta barrel scaffold.

Amino Acid Sequence↗
PubMed2003

Gas phase ion chemistry of charged silver(I) adenine ions via multistage mass spectrometry experiments and DFT calculations.

Electrospray ionization (ESI) of solutions containing adenine and AgNO(3) yields polymeric [Ad(x)+ Ag(y)-zH]((y-z)+) species. Density functional theory (DFT) calculations have been used to examine potential structures for several of the smaller ions while multistage mass spectrometry experiments have been used to probe their unimolecular reactivity (via collision-induced dissociation (CID)) and bimolecular reactivity (via ion-molecule reactions with the neutral reagents acetonitrile, methanol, butylamine and pyridine). DFT calculations of neutral adenine tautomers and their silver ion adducts provide insights into the binding modes of adenine. We find that the most stable [Ad + Ag](+) ion does not correspond to the most stable neutral adenine tautomer, consistent with previous studies that have shown that transition metal ions can stabilize rare tautomeric forms of nucleobases. Both the charge and the stoichiometry of the [Ad(x)+ Ag(y)-zH]((y-z)+) complexes play pivotal roles in directing the types of fragmentation and ion-molecule reactions observed. Thus, [Ad(2)+ Ag(2)](2+) is observed to dissociate to [Ad + Ag](+) and to react with butylamine via proton transfer, while [Ad(2)+ Ag(2)- H](+) fragments via loss of neutral adenine to form the [Ad + Ag(2)- H](+) ion and does not undergo proton transfer to butylamine. DFT calculations on several isomeric [Ad(2)+ Ag(2)](2+) ions suggest that planar centrosymmetric cations, in which two adjacent silver atoms are bridged by two N7H adenine tautomers via N(3),N(9)-bidentate interactions, are the most stable. The [Ad + Ag(2)-H](+) ion adds two neutral reagents in ion-molecule reactions, consistent with the presence of two vacant coordination sites. It undergoes a silver atom loss to form the [Ad + Ag - H](+) radical cation, which in turn fragments quite differently to the even electron [Ad + Ag](+) ion. Several other pairs of radical cation/even electron adenine-silver complexes were also found to undergo different fragmentation reactions.

Journal Article↗