Anion exchange and anion-cation co-transport systems in mammalian cells

Abstract

Electroneutral anion transfer in the Ehrlich ascites tumour cell has been found to occur by two separate mechanisms. One is an exchange diffusion system with many similarities to that found in erythrocytes, e.g. saturation kinetics with ‘self-inhibition’, a relatively pronounced temperature dependence, competitive interactions of Br- , NO - 3 and SCN- , and a low conductive P Cl - of 4 x 10 -8 cm s -1 . The main differences are that the Cl- flux in Ehrlich cells at 38 °C is one thousandth of the flux in red cells, and that the specificity of the system is less pronounced. It is suggested that the density of anion exchange sites in Ehrlich cells could be the same as in red blood cells, but with a lower turnover rate. The other system is an anion-cation co-transport system capable of mediating a secondary active Cl- influx. This system has a volume-regulatory function and is activated by a reduction in cell volume and intracellular [Cl-]. The two transport systems can be separated by using DIDS as an inhibitor of anion exchange and bumetanide as an inhibitor of co-transport. Under normal steady-state conditions Cl- flux is dominated by the exchange system. It is suggested that intracellular pH regulation can be achieved by the two systems operating in parallel, because the chloride disequilibrium maintained by the co-transport system can drive an influx of bicarbonate through the exchange mechanism.