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Nucleotide degradation

Schmatz R, Schetinger MR, Spanevello RM, Mazzanti CM, Stefanello N, Maldonado PA, Gutierres J, Correa Mde C, Girotto E, Moretto MB, Morsch VM. (2009) Effects of resveratrol on nucleotide degrading enzymes in streptozotocininduced diabetic rats. Life Sci 84 345-350. [Pg.594]

Figure 1. Nucleotide degradation pathway (ATP=adenosine-5 -triphosphate, ADP=adenosine-5 -diphosphate, AMP=adenosine-5 -monophosphate, IMP=inosine-5 -monophosphate). Figure 1. Nucleotide degradation pathway (ATP=adenosine-5 -triphosphate, ADP=adenosine-5 -diphosphate, AMP=adenosine-5 -monophosphate, IMP=inosine-5 -monophosphate).
To prevent possible nucleotide degradation when using TCA, Khym (K12) suggested the use of amine/Freon solution to back-extract excessive acid. Khym s procedure has been modified by Van Haverbeke and Brown (V3), and has been applied by others to the study of nucleotides (C3, R3, V3) and nucleosides (HIO). Similar to the results reported by Chen et al. (C3), Riss and co-workers (R3) reported that the recovery of the adenosine-, cytidine-, guanosine-, and uridine-5 -nucleotides range from 81 to 99%, with an average recovery of 91% (Table IV). [Pg.19]

Cyclic nucleotide degradative activity occurs in mammalian whole blood, but it is not known whether phosphodiesterase exists in plasma in vivo. The enzyme can be released from damaged platelets and granulocytes in vitro. However, degradation of cyclic AMP in whole blood is slowed by reduction in temperature, immediate centrifugation and addition of methylxanthines, and plasma can be pipetted directly into HCIO4. It is usually necessary to process several milliliters of plasma owing to the low cyclic nucleotide levels and losses with purification. [Pg.311]

Kuracka, L. Kalnovicova, T. Liska, B. Turcani, P. HPLC method for measurement of purine nucleotide degradation products in cerebrospinal fluid. Clin. Chem. 1996, 42 (5), 756-760. [Pg.469]

For many foods one of the most important quality criterion is freshness. This is especially so in numerous species of vegetables, fruits, and seafood. Fish of valuable species at the state of prime freshness, suitable to be eaten raw, may have a market price that is ten times higher than that of the same fish after several days of storage in ice but still very fit for human consumption. The characteristic freshness attributes of different foods are usually evaluated by sensory examination and by determination of specific indices, e.g., nucleotide degradation products in fish. [Pg.5]

Reutilization of purine bases after conversion to their respective nucleotides constitutes salvage pathways. These pathways are particularly important in extrahepatic tissues. Purines arise from several sources intermediary metabolism of nucleotides, degradation of polynucleotides, and dietary intake. Quantitatively, the first two sources are the more important. Salvage occurs mainly by the phosphoribosyltransferase reaction ... [Pg.622]

The answer is a. (Murray, pp 812—828. Scriver, pp 2537-2570. Sack, pp 97—158. Wilson, pp 287-320.) The child has Lesch-Nyhan syndrome (308000), an X-linked recessive disorder that is caused by HGPRT enzyme deficiency. HGPRT is responsible for the salvage ol purines from nucleotide degradation, and its deficiency elevates levels ol PRPP, purine synthesis, and uric acid. PRPP is also elevated in glycogen storage diseases due to increased amounts of carbohydrate precursors. [Pg.381]

Any excess nucleotide dNTP and any excess ATP are degraded by the nucleotide degrading enzyme apyrase to their respective mono-and diphosphates (Fig. 5.29). When degradation is complete, the next dNTP can be added. [Pg.138]

Fig. 5.29. The nucleotide degrading enzyme apyrase destroys any remaining dNTP and ATP. Fig. 5.29. The nucleotide degrading enzyme apyrase destroys any remaining dNTP and ATP.
Fig. 1 Metabolic pathways of purine metabolism showing the role of the salvage enzymes HGPRT and APRT and the alternative route of adenine metabolism when APRT is absent of inhibited. Adenine is not a product of purme nucleotide degradation in man but is produced as a by-product of the poly amine pathway. Fig. 1 Metabolic pathways of purine metabolism showing the role of the salvage enzymes HGPRT and APRT and the alternative route of adenine metabolism when APRT is absent of inhibited. Adenine is not a product of purme nucleotide degradation in man but is produced as a by-product of the poly amine pathway.
Purine analysis can be achieved with this system, specifically inosine (the co-substrate, with phosphate. Scheme 5.5) can be determined quantitatively using similar methodology. The hypoxanthine ratio ([hypoxanthine]/ [hypoxanthine] + [inosine] + [inosine-monophosphate]) is key measure of fish freshness as hypoxanthine is a product of nucleotide degradation and a sign of spoilage. As mentioned previously, hypoxanthine or xanthine... [Pg.192]

Ferro, A.M., Olivera, B.M. (1987) Intracellular Pyridine Nucleotide Degradation and Turnover in Pyridine Nucleotide Coenzymes Chemical, Biochemical and Medical Aspects, Vol. 2B D. Dolphin, R. Poulson, O. Avramovic (eds.) pp, 25-77... [Pg.360]

I. H. Fox, Metabolic basis for disorders of purine nucleotide degradation Metabolism. 30 616 (1981). [Pg.252]

S.S. Matsumoto, K.O. Raivio and J.E. Seegmiller, Adenine nucleotide degradation during energy depletion in human lymphoblasts adenosine accumulation and adenylate energy charge correlation. [Pg.358]

These data confirm that at this rate of ethanol administration, uric acid excretion did not decrease. The increased excretion of uric acid precursors suggests, in fact, that there is increased flux through the pathways of purine nucleotide degradation to uric acid. Excretion of labeled degradation products derived from the adenine nucleotide pool is significantly accelerated and suggests accelerated ATP or adenine nucleotide degradation. [Pg.461]

In recent years it became apparent that fructose metabolism in the liver tissue has considerable effects on purine nucleotide metabolism. There is ample evidence that fructose metabolism is associated with acceleration of nucleotide degradation (1-5) and evidence is accumulating (6-8), indicating an acceleration effect of fructose also on purine synthesis. [Pg.481]

Adenosine is an intermediate of the pathway of purine nucleotide degradation. Many biological properties of adenosine have been identified It is toxic to mammalian and bacterial cells, and its... [Pg.497]


See other pages where Nucleotide degradation is mentioned: [Pg.217]    [Pg.186]    [Pg.419]    [Pg.251]    [Pg.343]    [Pg.495]    [Pg.560]    [Pg.356]    [Pg.536]    [Pg.280]    [Pg.38]    [Pg.463]    [Pg.1429]    [Pg.573]    [Pg.163]    [Pg.505]    [Pg.524]    [Pg.524]    [Pg.526]    [Pg.270]    [Pg.423]    [Pg.460]    [Pg.461]    [Pg.484]    [Pg.338]    [Pg.247]   
See also in sourсe #XX -- [ Pg.187 , Pg.419 ]

See also in sourсe #XX -- [ Pg.119 ]

See also in sourсe #XX -- [ Pg.206 ]




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