Electrophysiological evidence for the herbicidal mode of action of phosphonic acid esters

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Abstract
The electrical membrane potential of leaf cells of the higher aquatic plant Egeria densa Planchon, measured with microelectrodes, was immediately depolarized after treatment with 0.29 mM of the dialkyl phosphonic ester, O, O‐di‐n‐butyl‐(1‐n‐butylamino‐cyclohexyl)‐phosphonate (PABT). This depolarization was followed by a strong electrolyte efflux after ca 90 min. Active photosynthesis or respiration as well as an intact plasma membrane was essential for this effect. An increased concentration of thiobarbituric acid (TBA)‐reactive agents observed within this period suggests that membrane destruction by lipid peroxidation was responsible for the electrolyte efflux. Antioxidants such as α‐tocopherol (0.25 mM) and ascorbic acid (1 mM) stopped electrolyte efflux, but did not affect the depolarization.Fusicoccin (1 μM) prevented PABT‐induced membrane depolarization and the subsequent electrolyte efflux. Also, the ATPase inhibitor, DES (50 üM), as well as substances which stimulate the proton pump such as sucrose (30 mM), AIB (10 μM), and acetate (1 mM), prevented PABT‐mediated electrolyte efflux. The depolarizing effect of PABT was also obviated above pH 7.5. Thus, if the PABT‐induced depolarization was inhibited no membrane destruction occurred whereas depolarization alone was not a sufficient condition for the development of the PABT action. The initial depolarizing effect of PABT cannot be explained by a physical interaction with the lipid part of the plasma membrane. Thus, a metabolism‐driven mode of action connected to plasma membrane energization has to be assumed.