The effects of sodium ions and potassium ions on glycine uptake by mouse ascites-tumour cells in the presence and absence of selected metabolic inhibitors.

1. The initial rate, v, of glycine uptake by ascites-tumour cells respiring their endogenous nutrient reserves was studied as a function of the respective extracellular concentrations of glycine, Na(+) and K(+). With the extracellular concentration of Na(+)+K(+) constant at 158m-equiv./l. and that of glycine either 4 or 12mm, v tended to zero as the extracellular concentration of Na(+) approached zero. Glycine appeared to enter the cells as a ternary complex with a carrier and Na(+). K(+) competed with Na(+) for one of the carrier sites, whereas glycine was bound at a second site. The values of the five relevant binding constants showed that the two sites interacted. 2. The glycine uptake rate at various extracellular concentrations of glycine and Na(+) was scarcely affected by starving the cells for 30min. in the presence of 2mm-sodium cyanide provided that cellular Na(+) and K(+) contents were kept at the normal values. When the cells took up Na(+), however, v decreased approximately threefold. 3. When their Na(+) content was relatively small and the extracellular concentration of Na(+) was large, the starved cells accumulated glycine in the presence of cyanide for about 15min. Glycine then tended to leave the cells. An average of about 5mumoles of glycine/ml. of cell water was taken up from a 1mm solution, representing about 20% of the accumulation observed during respiration. Studies with fluoride, 2,4-dinitrophenol and other metabolic inhibitors supported the view that ATP and similar compounds were not implicated. The relation between the transient accumulation of glycine that occurred in these circumstances and the normal mode of active transport was not established.