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 long-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 short-term copper-induced K(+) efflux. In contrast, peroxide-induced K(+) efflux was insensitive to both tetraethyl ammonium chloride and 4-AP. Copper-induced lipid peroxidation exhibited a lag time of 4 h, while peroxide-induced lipid peroxidation began immediately. These results suggest that short-term copper-induced K(+) efflux is mediated by channels, while peroxide-induced K(+) efflux represents leakage through nonspecific lesions in the lipid bilayer. Tracer studies with (86)Rb(+) confirmed that copper promotes K(+) efflux rather than inhibiting K(+) uptake. Short-term K(+) release is electroneutral, since electrophysiological measurements indicated that copper does not cause membrane depolarization. Short-term K(+) efflux was accompanied by citrate release, and copper increased total citrate levels. Since citrate efflux was blocked by 4-AP, K(+) appears to serve as a counterion during copper-induced citrate efflux. As copper but not aluminum selectively induces citrate production and release, it is proposed that copper may inhibit a cytosolic form of aconitase.