The effect of glycine transport on potassium fluxes in the Ehrlich mouse ascites tumor cell.

Christensen, Riggs, and their coworkers (l-5) showed that the Ehrlich mouse ascites tumor cell concentrated amino acids to values many times that of the environment. Glycine, for example, was concentrated to 16 times that of the external solution. Heinz (6-8) studied the kinetics of glycine accumulation and showed that active transport across the cell membrane was responsible for the concentration ratios observed. In addition, Heinz’s data provided evidence for exchange diffusion of glycine for glycine or other amino acids for glycine (6). From their studies, Christensen and Riggs correlated amino acid transport with potassium movements and advanced the hypothesis that “amino acid uptake could conceivably be driven wholly by the energy inherent in the asymmetry of cellular alkali distribution.” One mechanism suggested was that potassium c6lux drove glycine influx by exchange diffusion (5). Their experiments, however, were not designed to assess potassium fluxes. Rather, they correlated net changes in cell potassium with concentration ratios of amino acids. Since correlations need not imply causal relations, it was the purpose of our experiments to measure the potassium fluxes with Ku under circumstances in which the cells had already established glycine gradients, or were in the process of taking up glycine. We found that both influx and efflux of potassium increased when the cells were maintaining established gradients for glycine; both fluxes also increased during the accumulation of glycine. However, potassium efflux does not drive glycine accumulation because more free energy is required for glycine accumulation than is available from potassium efflux. It is more likely that either potassium plays a permissive role in glycine accumulation or that glycine accumulation facilitates potassium transport.