OXIDATION OF GLUCOSE AND OTHER SUBSTRATES BY EHRLICH ASCITES TUMOR CELLS

The time courses of oxidation of pyruvate-3-14C and of palmitate-16-14C to 14CO2 in Ehrlich ascites cells are qualitatively and quantitatively similar when expressed in terms of units of acetyl-CoA oxidized. The time courses of oxidation of pyruvate-2-14C and of palmitate-1-14C are also similar to each other, but the delay preceding the attainment of a steady state rate of oxidation is of shorter duration. Similarly, the delay preceding the oxidation of glucose-2-14C at a constant rate is significantly less than the corresponding delay for glucose-6-14C. There is little or no delay with pyruvate-1-14C or giucose-1-14C. All compounds giving rise to acetyl-CoA labeled in the methyl group yield 14CO2 more slowly than the corresponding compounds in which the acetyl-CoA produced is labelled in the carbonyl moiety. Studies with labeled lactate suggest that as the concentration of lactate increases through glycolysis (and therefore also the concentration of pyruvate) its rate of oxidation increases and an increased rate of production of 14CO2 from labeled glucose is to be expected. The reason for the long delay preceding the oxidation of glucose-6-14C is hence to be explained partly on the basis of the formation of acetyl-CoA labeled in the methyl moiety and partly because the 14CO2 produced is derived from lactate and pyruvate which are present at increasing concentrations throughout the experimental period.The rate of oxygen uptake observed when Ehrlich ascites carcinoma cells are incubated with dinitrophenol (DNP) plus glucose, pyruvate, or glutamine is high and is the same for each of these three substrates. It is suggested that, in the presence of glucose, the effect of DNP is to cause oxidation of exogenous substrates rather than to reverse the Crabtree effect.