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Adenosine triphosphate metabolism

Adenosine is not active orally, but adrninistered as an iv bolus dmg adenosine rapidly eliminates supraventricular tachycardias within 1—2 min after dosing. The dmg slows conduction through the AV node. Adenosine is rapidly removed from the circulation by uptake into red blood ceUs and vascular endothehal ceUs. Thus the plasma half-life is less than 10 s. Adenosine is rapidly metabolized to inosine or adenosine monophosphate and becomes part of the body pool for synthesis of adenosine-triphosphate. [Pg.120]

Phosphate condensation reactions play an essential role in metabolism. Recall from Section 14.6 that the conversion of adenosine diphosphate (ADP) to adenosine triphosphate (ATP) requires an input of free energy ADP -I-H3 PO4 ATP +H2O AG° — +30.6kJ As also described in that section, ATP serves as a major biochemical energy source, releasing energy in the reverse, hydrolysis, reaction. The ease of interchanging O—H and O—P bonds probably accounts for the fact that nature chose a phosphate condensation/hydrolysis reaction for energy storage and transport. [Pg.1530]

Adenosine triphosphate (ATP) The principal chemical energy source for cellular processes. It is largely produced during aerobic metabolism. In the neuron most ATP is used in the maintenance of the electrochemical gradient required to generate an action potential. [Pg.235]

Only a few years after the Miller-Urey experiment was published, J. Oro was able to synthesize one of the most important biomolecules, adenine. This purine derivative is not only a component of the nucleic acids, but as ATP, adenosine triphosphate (in combination with ribose and three phosphate residues), it plays a key role in the metabolism of all living creatures. The chemical formula of adenine is C5H5N5, or expressed in another way, (HCN)s. [Pg.92]

F. H. Westheimer (1987) has provided a detailed survey of the multifarious ways in which phosphorus derivatives function in living systems (Table 4.7). The particular importance of phosphorus becomes clear when we remember that the daily turnover of adenosine triphosphate (ATP) in the metabolic processes of each human being amounts to several kilograms Phosphate residues bond two nucleotides or deoxynucleotides in the form of a diester, thus making possible the formation of RNA and DNA the phosphate always contains an ionic moiety, the negative charge of which stabilizes the diester towards hydrolysis and prevents transfer of these molecules across the lipid membrane. [Pg.115]

About 10% of the acid-soluble phosphorus of the red blood cells in galactosemia is accounted for by galactose-l-phosphate. Since all this is derived from adenosine triphosphate by reaction (1), it represents the tying up in a metabolically useless form of a high proportion of the high-energy phosphate of the erythrocyte. Untreated galactosemics have... [Pg.34]

Two important implications of the reactions described in Equations (5.1) and (5.2) are (i) that redox reactions play an important role in metabolic transformations, with the cofactors nicotinamide adenine dinucleotide (NAD+) acting as electron acceptor in catabolic pathways and nicotinamide adenine dinucleotide phosphate (NADPH) as electron donor in anabolism, and (ii) that energy must be produced by catabolism and used in biosyntheses (almost always in the form of adenosine triphosphate, ATP). [Pg.78]

In the past decade, a large number of studies emphasized the heterogeneous scale-free degree distribution of metabolic networks Most substrates participate in only a few reactions, whereas a small number of metabolites ( hubs ) participate in a very large number of reactions [19,45,52]. Not surprisingly, the list of highly connected metabolites is headed by the ubiquitous cofactors, such as adenosine triphosphate (ATP), adenosine diphosphate (ADP), and nicotinamide adenine dinucleotide (NAD) in its various forms, as well as by intermediates of glycolysis and the tricarboxylic acid (TCA) cycle. [Pg.153]

Adenosine Triphosphate Adenosine 5 -(tetrahydrogen triphosphate). An adenine nucleotide containing three phosphate groups esterified to the sugar moiety. In addition to its crucial roles in metabolism adenosine triphosphate is a neurotransmitter. [NIH]... [Pg.60]

Microbial activity requires energy, and all microorganisms generate energy. This energy is subsequently stored as adenosine triphosphate (ATP), which can then be utilized for growth and metabolism as needed, subject to the second law of thermodynamics [2,23,35,41,42,51,54]. [Pg.326]

Other nuclei, such as 13C or 31P, may be used to study other metabolite pools, or they can complement H-NMR to create more sophisticated NMR spectra. 13C-NMR provides a greater spectral range ( 200 ppm) than H-NMR ( 15 ppm). Although lower natural abundance of 13C (1.1%) yields lower sensitivity, it also provides an opportunity to use isotopic enrichment to trace specific metabolic pathways with enhanced sensitivity.4 31P can observe high-energy phosphate metabolites such as adenosine triphosphate. [Pg.192]

Adenosine (Adenocard) is an endogenous nucleoside that is a product of the metabolism of adenosine triphosphate. It is used for the rapid termination of supraventricular arrhythmias following rapid bolus dosing. [Pg.192]

Schematic illustration of a generalized cholinergic junction (not to scale). Choline is transported into the presynaptic nerve terminal by a sodium-dependent choline transporter (CHT). This transporter can be inhibited by hemicholinium drugs. In the cytoplasm, acetylcholine is synthesized from choline and acetyl -A (AcCoA) by the enzyme choline acetyltransferase (ChAT). Acetylcholine is then transported into the storage vesicle by a second carrier, the vesicle-associated transporter (VAT), which can be inhibited by vesamicol. Peptides (P), adenosine triphosphate (ATP), and proteoglycan are also stored in the vesicle. Release of transmitter occurs when voltage-sensitive calcium channels in the terminal membrane are opened, allowing an influx of calcium. The resulting increase in intracellular calcium causes fusion of vesicles with the surface membrane and exocytotic expulsion of acetylcholine and cotransmitters into the junctional cleft (see text). This step can he blocked by botulinum toxin. Acetylcholine s action is terminated by metabolism by the enzyme acetylcholinesterase. Receptors on the presynaptic nerve ending modulate transmitter release. SNAPs, synaptosome-associated proteins VAMPs, vesicle-associated membrane proteins. Schematic illustration of a generalized cholinergic junction (not to scale). Choline is transported into the presynaptic nerve terminal by a sodium-dependent choline transporter (CHT). This transporter can be inhibited by hemicholinium drugs. In the cytoplasm, acetylcholine is synthesized from choline and acetyl -A (AcCoA) by the enzyme choline acetyltransferase (ChAT). Acetylcholine is then transported into the storage vesicle by a second carrier, the vesicle-associated transporter (VAT), which can be inhibited by vesamicol. Peptides (P), adenosine triphosphate (ATP), and proteoglycan are also stored in the vesicle. Release of transmitter occurs when voltage-sensitive calcium channels in the terminal membrane are opened, allowing an influx of calcium. The resulting increase in intracellular calcium causes fusion of vesicles with the surface membrane and exocytotic expulsion of acetylcholine and cotransmitters into the junctional cleft (see text). This step can he blocked by botulinum toxin. Acetylcholine s action is terminated by metabolism by the enzyme acetylcholinesterase. Receptors on the presynaptic nerve ending modulate transmitter release. SNAPs, synaptosome-associated proteins VAMPs, vesicle-associated membrane proteins.

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