UPTAKE OF GLUFOSINATE AND CONCOMITANT MEMBRANE-POTENTIAL CHANGES IN LEMNA-GIBBA G1

Uptake of the herbicide glufosinate (PPT) in Lemna gibba proceeded biphasically with respect to time and concentration. Addition of PPT caused a primary electrical depolarization of the plasmalemma similar to that by glutamate, but without or with only incomplete recovery in the presence of PPT and superimposed by a slower, secondary depolarization. After any treatment with PPT, even if the membrane potential had completely recovered, responses to glutamate were severely reduced. Uptake of PPT was stimulated by light, while membrane depolarization was not different between light and dark. PPT uptake was strongly enhanced below pH 5, but remained unchanged between pH 5 and 7. By addition of PPT together with glutamate or alanine the PPT uptake rate and the rate of secondary depolarization were reduced. When added simultaneously with PPT, even glucose caused some inhibition of uptake. If PPT was added after but in the presence of glutamate, alanine, or glucose only the amino acids caused a partial inhibition of PPT uptake, the primary depolarization by PPT was completely suppressed and the secondary depolarization much reduced. PPT and glutamate uptake caused an increase in extracellular pH due to their uptake as strongly dissociated anions. Concomitantly, PPT induced a continuous K+ release; glutamate instead, after some release, an enhanced net K+ reabsorption. Because of its immediate membrane-depolarizing effect the anion PPT is assumed to be taken up by a proton cotransport mechanism, using the same carrier as neutral and acidic amino acids. At low pH, additional undissociated acid is transported by diffusion. The secondary depolarization is attributed to diminished energy supply due to uncoupling by accumulated ammonium and to direct interference with the membranes. This is revealed by the irreversible inhibition of glutamate/H+ cotransport and by increasing K+ efflux. © 1990.