Abstract
Genetic deficienceis in the nucleoside transport function markedly altered the abilities of cultured mutant S49 T lymphoblasts to transport, incorporate, and salvage exogenous hypoxanthine. The concentrations of hypoxanthine required to reverse azaserine toxicity and replenish azaserine-depleted nucleoside triphosphate pools in AE1 cells, a nucleoside transport-deficient clone, were about 10-fold higher than those required for wildtype cells. Surprisingly, a second nucleoside transport-deficient clone, 80-5D2, which had lost 80-90% of its ability to transport nucleosides, required lower hypoxanthine concentrations to reverse these azaserine-mediated effects. The addition of 10μM p-nitrobenzylthioinosine (NBMPR), a potent inhibitor of nucleoside transport, to wildtype cells mimicked the phenotype of the AE1 cells with respect to the hypoxanthine reversal of the effects of azaserine. AE1 cells or NBMPR-treated wildtype cells could only transport hypoxanthine at 20% the rate of untreated wildtype cells The 80-5-D2 cell line could transport and utilize hypoxanthine more efficiently than the wildtype parental cell line. A genetic deficiency in nucleoside transport did not interfere with adenine transport, incorporation, or salvage, however. These studies on S49 T lymphoblasts altered in their nucleoside transport capacity provide powerful genetic evidence that hypoxanthine and nucleosides share a common transport function.
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Aronow, B., Ullman, B. ROLE OF THE NUCLEOSIDE TRANSPORT FUNCTION IN THE TRANSPORT, INCORPORATION, AND SALVAGE OF HYPOXANTHINE: 5. Pediatr Res 19, 744 (1985). https://doi.org/10.1203/00006450-198507000-00025
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DOI: https://doi.org/10.1203/00006450-198507000-00025