Conclusion
The higher specific radioactivity of ALL in comparison to UA, which are observed after administration of labelled precursors, changed when, oxonic acid and allopurinol, inhibitors of UA and ALL formation were administrated. To interpret these results, it is worth while to recall that nucleotide metabolism can be represented as a complex sequence including de novo synthesis of nucleotides and their degradation to UA and ALL. UA is both partially exported to the blood and partially transformed into ALL, which is totally exported to the blood. Under normal conditions, the radioactivity of UA and ALL is similar, in the case of14 C-glycine, while in the other cases (after 14C-formate and other precursors), the formation of ALL is so fast, that it exceedes export from liver to serum, and the radioactivity of the precursors accumulates in ALL. When we treated with the oxonic acid and allopurinol, formation of ALL was reduced, became slower than its export, leading to a higher labelling into UA.
A partial explanation of our results is that the radioactivity of precursors will accumulate into ALL, depending on the rate they are inserted into UA and on the point in which they are inserted in the sequence of the de novo synthesis.
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© 2002 Kluwer Academic Publishers
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Marinello, E., Pagani, R., Arezzini, L., Porcelli, B., Cinci, G., Terzuoli, L. (2002). Purine Nucleotide Catabolism in Rat Liver. In: Zoref-Shani, E., Sperling, O. (eds) Purine and Pyrimidine Metabolism in Man X. Advances in Experimental Medicine and Biology, vol 486. Springer, Boston, MA. https://doi.org/10.1007/0-306-46843-3_20
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