Add time:07/20/2019         Source:sciencedirect.com

6-N-Hydroxylaminopurine (HAP) prolonged the survival time of mice bearing sarcoma 180 ascites cells; several other ascitic neoplasms were less sensitive to this agent. The rate of incorporation of 2-14C-glycine into both polynucleotide adenine and guanine of sarcoma 180 was depressed 90% or more by treatment with HAP, and the utilization of 8-14C-hypoxanthine and 8-14C-adenine for nucleotide formation was decreased by approximately 85% and 50% respectively. HAP competitively inhibited the formation of adenylic acid from adenine in cell-free extracts of sarcoma 180; the inhibition of inosinic acid formation from hypoxanthine by this analog was complex, being only partially competitive.Dialyzed extracts of either sarcoma 180 or of a variant resistant to purine analogs formed nucleotide from HAP at similar rates, whereas extracts of the L1210 lymphoma formed 5.6-fold more HAP-nucleotide than did those from a 6-mercaptopurine-resistant subline. The extracts from drug-sensitive and -resistant L1210 cells converted adenine to the nucleotide level at equal rates ; only the susceptible neoplasm converted guanine to guanylic acid at a significant rate. In cultured 14L5178Y lymphoblasts, capable of synthesizing purine nucleotides de novo, both hypoxanthine and adenine prevented inhibition of cell reproduction by HAP; on a molar basis adenine was the more effective. In amethopterin-treated L5178Y cells, high levels of HAP supported cell growth in the presence of thymidine and serine. The results suggest that HAP may function as both an antagonist of adenine and hypoxanthine in mammalian cells. Furthermore, the inhibition of cell reproduction caused by this compound appears to be attributable to interference with the biosynthesis of purine nucleotides.

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