Deoxycytidine is salvaged not only into DNA but also into phospholipid precursors. II. Ara-C does not inhibit the later process in lymphoid cells.

dCTP formed from exogenous deoxycytidine via the salvage pathways was previously shown to serve deoxyliponucleotide synthesis in lymphocytes (Spasokukotskaja et al, Biochem. Biophys. Res. Commun. (1988) 155, 923-929) and now in lymphoma cells. After treatment with 1-beta-D-arabino-furanosylcytosine (ara-C), much more araCTP as well as araCDP-choline was formed in lymphoma cells than in lymphocytes explaining the high sensitivity of lymphoma cells to this drug. Ara-C did not inhibit labeling of 5-3H-dCDP-choline from exogenous 5-3H-deoxycytidine while inhibiting DNA synthesis. Excess of exogenous ribocytidine diminished labeling of araCDP-choline, without any effect on dCDP-choline. These data suggest that araCDP-choline and dCDP-choline were synthesized from separate pools in these cells.