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 formulafton of diclofop, at 0.2 micromolar, completely inhibited root growth in herbicide-susceptible oat (Avena Lucas et al. (16) and later revised by Wright and Shimabukuro (25), the ester form of diclofop crosses the plasmalemma and is rapidly hydrolyzed to the free acid form. This undissociated acid then releases a proton on the cytoplasmic side of the membrane. The deprotonated anionic species then moves back across the plasmalemma to the apoplasmic side in response to the root-cell Em (inside negative) and is again protonated. This cycle is repeated until the proton gradient is dissipated and could eventually lead to a reduction in cellular ATP levels by short circuiting the proton-translocating plasmalemma ATPase. The diclofop concentration causing half-maximal depolarization of the Em in excised and peeled oat coleoptiles was determined to be 10 to 20 jtM (25). Ratterman and Balke (20)

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