Purine excretion by mammalian cells deficient in adenosine kinase

Teh‐Sheng ‐S Chan, Kazuhiro Ishii, Cedric Long, Howard Green

Research output: Contribution to journalArticle

46 Scopus citations

Abstract

An adenosine kinaseless (AK) mutant of the mouse fibroblast line 3T6 has been obtained in cell culture by evolution of resistance to 6‐thio‐methylpurine ribonucleoside and tubercidin. The mutant excretes purines (xanthine and hypoxanthine) into the culture medium. Human or mouse cells lacking hypoxanthine‐guanine phosphoribosyl transferase (HPT) excrete increased amounts of purines, but a human cell mutant lacking both HPT and AK excretes considerably more hypoxanthine. The difference in hypoxanthine excretion between the HPT mutant and the HPT AK mutant originates from the adenosine normally reutilized through the activity of adenosine kinase. The activity of adenosine kinase is essential to retard the adenosine cycle and to prevent cellular loss of purines.

Original languageEnglish (US)
Pages (from-to)315-321
Number of pages7
JournalJournal of Cellular Physiology
Volume81
Issue number3
DOIs
StatePublished - Jun 1973

ASJC Scopus subject areas

  • Physiology
  • Clinical Biochemistry
  • Cell Biology

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