Control of adenosine monophosphate catabolism in mouse ascites tumor cells.

Experiments were conducted to determine whether en ergy charge, (ATP + 1/2 ADP)/(ATP + ADP + AMP) (in which AMP, ADP, and ATP are adenosine mono-, di-, and triphosphate, respectively) or intracellular inorganic phosphate was the primary regulator of the rate of aden osine 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 NaCI, 5.5 mwi KCI, and 10 nriMN-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 treat ments 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 ¿imol/mlof cells. A normal or increased intracellular phosphate con centration (7 to 15 /¿mol/mlof cells) abolished AMP catabolism. No consistent relationship was noted be tween the energy charge value and the rate of adenine nucleotide catabolism, and it was concluded that the in organic phosphate content is the primary regulator of AMP catabolism in mouse ascites tumor cells.