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Control of Adenosine Monophosphate Catabolism in Mouse Ascites Tumor Cells¹

The Mary Imogene Bassett Hospital, Cooperstown, New York 13326

Experiments were conducted to determine whether energy charge, (ATP + 1/2 ADP)/(ATP + ADP + AMP) (in which AMP, ADP, and ATP are adenosine mono-, di-, and triphosphate, respectiviely) or intracellular inorganic phosphate was the primary regulator of the rate of adenosine 5'-monophosphate (AMP) catabolism in intact mouse ascites tumor cells. Hyperdiploid (ELD) and tetraploid (ELT/B1) cell suspensions were incubated in vitro in a solution containing 0.15 M NaCl, 5.5 mM KCI, and 10 mM N-2-hydroxyethylpiperazine-N'-2-ethanesulfonic acid buffer. The suspensions were treated with glucose, with 2-deoxyglucose, with an uncoupler of oxidative phosphorylation, and with an aerobic-anaerobic transition. Intracellular inorganic phosphate and the adenine nucleotides were measured at several time points. These treatments increased intracellular AMP, decreased the energy charge, and either decreased or increased intracellular inorganic phosphate. AMP catabolism occurred only if the intracellular phosphate decreased to 1 to 2 µmol/ml of cells. A normal or increased intracellular phosphate concentration (7 to 15 µmol/ml of cells) abolished AMP catabolism. No consistent relationship was noted between the energy charge value and the rate of adenine nucleotide catabolism, and it was concluded that the inorganic phosphate content is the primary regulator of AMP catabolism in mouse ascites tumor cells.

¹ This research was supported by NIH Grants CA 13610 and CA 17450 and by the Stephen Cariton Clark Research Fund of The Mary Imogen Bassett Hospital. Part of this work was presented at the 61st Annual Meeting of the Federation of American Societies for Experimental Biology, Chicago, III., April 1 to 8, 1977 (28).

Received 10/ 3/77. Accepted 1/ 3/78.