HGCL2-INDUCED ION-TRANSPORT PATHWAYS IN EHRLICH ASCITES TUMOR-CELLS

HgCl2 (40 muM) initially activates an anion-independent unidirectional Na+ influx in Ehrlich ascites tumor cells, which amounts to 61 +/- 7 mumol.g dry wt-1.min-1 (+/- SEM, n = 5). The unidirectional Na+ influx in control cells in 13 +/- 2 mumol.dry wt-1.min-1 (+/- SEM, n = 5). The HgCl2-activated Na+ influx is slightly inhibited by amiloride (inhibitor of Na+/H+ exchange), but almost completely blocked by the anion-exchange inhibitor DIDS (4,4'-diisothiocyano-2,2'-stilbenedisulfonic acid). HgCl2 also causes DIDS-sensitive cytoplasmic acidification followed by DIDS-sensitive cytoplasmic alkalinization. After addition of HgCl2 the cells initially shrink, whereupon they swell again. Half-maximal effect of HgCl2 is obtained with about 0.5 and 1 muM HgCl2 on cell swelling and cell shrinkage, respectively. The volume responses are both reduced in the presence of DIDS. The unidirectional K+ and Cl- effluxes are greatly stimulated by HgCl2. The stimulation of K+ efflux results in a Cl--dependent net loss of K+. In Cl- medium the K+ loss is 84 +/- 11 mumol.g dry wt-1.min-1 (+/- SEM, n = 6). In NO3- medium, it is reduced to 24 +/- 6 mumol.g dry wt-1.min-1 (+/- SEM, n = 4). The HgCl2 activated K+ efflux in Cl- medium is reduced to 21 +/- 6 mumol.g dry wt-1.min-1 (+/- SEM, n = 3) by DIDS. Finally, an instantaneous hyperpolarization of the cell membrane potential was observed after addition of HgCl2. It is concluded that HgCl2 in Ehrlich cells activates (i) a DIDS-sensitive, Na+-dependent anion exchange system; (ii) a DIDS-sensitive and anion-dependent K+ transport system, and (iii) K+ channels.