HgCI<sub>2</sub>-lnduced Ion Transport Pathways in Ehrlich Ascites Tumor Cells

Abstract

HgCl2 (40 µM) initially activates an anion-independent unidirectional Na+ influx in Ehrlich ascites tumor cells, which amounts to 61 ± 7 µmol·g dry wt-1 min-1 (± SEM, n = 5). The unidirectional Na+ influx in control cells in 13 ± 2 µmol·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 µM 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 µmol·g dry wt–1 • min–1 ( ± SEM, n = 6). In NO–3 medium, it is reduced to 24 ± 6 µmol·g dry wt-1 • min-1 ( ± SEM, n = 4). The HgCl2 activated K+ efflux in Cl– medium is reduced to 21 ± 6 µmol·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.