Effects of diclofop and diclofop-methyl on membrane potentials in roots of intact oat, maize, and pea seedlings.

Growth and electrophysiological studies in roots of intact diclofop-methyl susceptible and resistant seedlings were conducted to test the hypothesis that the herbicide acts primarily as a proton ionophore. The ester formulation of diclofop, at 0.2 micromolar, completely inhibited root growth in herbicide-susceptible oat (Avena sativa L.) after a 96 hour treatment, but induced only a delayed transient depolarization of the membrane potential in oat root cortical cells. Root growth in susceptible maize (Zea mays L.) seedlings was dramatically reduced by exposure to 0.8 micromolar diclofop-methyl, while the same diclofop-methyl exposure hyperpolarized the membrane potential within 48 hours after treatment. Furthermore, exposure of maize roots to the protonophore, carbonyl cyanide m-chlorophenylhydrazone (CCCP) (50 nanomolar), inhibited growth by only 31%, 96 hours after treatment, while the same CCCP exposure depolarized the resting potential by an average of 32 millivolts. Thus, the protonophore hypothesis cannot account for a differential membrane response to phytotoxic levels of diclofop-methyl in two susceptible species. From the results of others, much of the evidence to support the protonophore hypothesis was obtained using high concentrations of diclofop acid (100 micromolar). At a similar concentration, we also report a rapid (3 minute) diclofop-induced depolarization of the membrane potential in roots of susceptible oat and maize, moderately tolerant barley (Hordeum vulgare L.), and resistant pea (Pisum sativum L.) seedlings. Moreover, 100 micromolar diclofop acid inhibited growth in excised cultured pea roots. In contrast, 100 micromolar diclofop-methyl did not inhibit root growth. Since the membrane response to 100 micromolar diclofop acid does not correspond to differential herbicide sensitivity under field conditions, results obtained with very high levels of diclofop acid are probably physiologically irrelevant. The results of this study suggest that the effect of diclofop-methyl on the membrane potentials of susceptible species is probably unrelated to the primary inhibitory effect of the herbicide on plant growth.