Early copper-induced leakage of K+ from Arabidopsis seedlings is mediated by ion channels and coupled to citrate efflux

Copper tolerance among Arabidopsis ecotypes is inversely correlated with lo ng-term K+ leakage and positively correlated with short-term K+ leakage (A. Murphy, L. Taiz [1997] New Phytol 136:211-222). To probe the mechanism of the early phase of K+ efflux, we tested various channel blockers on copper and peroxide-induced K+ efflux from seedling roots. The K+ channel blockers tetraethyl ammonium chloride and 4-aminopyridine (4-AP) both inhibited sho rt-term copper-induced K+ efflux. In contrast, peroxide-induced K+ efflux w as insensitive to both tetraethyl ammonium chloride and 4-AP. Copper-induce d lipid peroxidation exhibited a lag time of 4 h, while peroxide-induced li pid peroxidation began immediately. These results suggest that short-term c opper-induced K+ efflux is mediated by channels, while peroxide-induced Kefflux represents leakage through nonspecific lesions in the lipid bilayer. Tracer studies with Rb-86(+) confirmed that copper promotes K+ efflux rath er than inhibiting K+ uptake. Short-term K+ release is electroneutral, sinc e electrophysiological measurements indicated that copper does not cause me mbrane depolarization. Short-term K+ efflux was accompanied by citrate rele ase, and copper increased total citrate levels. Since citrate efflux was bl ocked by 4-AP, K+ appears to serve as a counterion during copper-induced ci trate efflux. As copper but not aluminum selectively induces citrate produc tion and release, it is proposed that copper may inhibit a cytosolic form o f aconitase.