JBC, Vol. 252, Issue 6, 2010-2016, Mar, 1977

Exit transport of a cyclic nucleotide from mouse L-cells

P. G. Plagemann and J. Erbe

At a concentration of 30 mum, 1,4,5,6,8-pentazaacenaphthylene, 3-amino-1,5-dihydro-5-methyl-1-beta-D-[5-14C]ribofuranosyl (NSC-154020), a tricyclic, 7-deazapurine nucleoside (TCN) is rapidly taken up by cultured mouse L-cells and converted to intracellular TCN-monophosphate, but not further metabolized. The TCN-monophosphate is also excreted by the cells into the medium. It is released by a saturable process against a concentration gradient and the release is inhibited by various inhibitors of energy production. This inhibition correlates with a depletion of the cells of ATP. Thus TCN-monophosphate excretion probably involves an active transport system. This transport system is highly temperature-dependent (the Q10 falls between 3 and 4) and is inhibited by papaverine, theophylline, Persantin, Probenecid, phenethyl alcohol and p-chloromercuribenzoate, but not by 500 muM cyclic AMP, AMP, or adenosine. Significant amounts of various natural phosphorylated intermediates (AMP, ATP, UTP, UMP, UDP-hexoses, and phosphorylcholine) are not released from the cells under similar experimental conditions either in the absence or presence of 30 muM TCN.
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