The electrical resting potential across the plasmalemma of Lemna gibba L. (G 1) cells is −230 to −250 mV and the diffusion potential in the presence of 1 mol m−3 KCN + 1 mol m−3 salicylhydroxamic acid is about −100 mV. A concentration of 0.01 mol m−3 HgCl2 depolarises the transmembrane electrical potential in a largely reversible way. When the cells after 16 min of HgCl2‐application are returned to Hg‐free solution, the transmembrane electrical potential is only depolarised by 24 × 13 mV (SD, n = 13) compared with the potential prior to HgCl2 treatment. In contrast, a 16 min pretreatment with HgCl2 followed by a wash with mercury‐free solution reduces the transient depolarisations of transmembrane potential observed after addition of 5 mol m−3 D‐glncose or 1 mol m−3 L‐alaoine to about 60% of controls. These transient depolarisations are due to the onset of solute uptake. Accordingly, HgCl2‐pretreatment inhibits uptake of 14C‐3‐O‐methyl‐d‐glucose by more than 50% and uptake of 14C‐l‐alanine by more than 70%. Washing with 1 mol m−3 1,4‐dithiothreitol does not reverse this inhibition. It is, therefore, concluded that Hg2+ irreversibly binds to essential SH‐groups of the H+‐hexose and the H+‐amino‐acid cotransport carriers of Lemna gibba and inhibits these carriers without appreciably affecting the electrogenic proton‐extrusion pump.