Herbicidal activity of aryloxyphenoxypropionate and cyclohexanedione herbicides (graminicides) has been proposed to involve two mechanisms: inhibition of acetyl-coenzyme A carboxylase (ACCase) and depolarization of cell membrane potential. We examined the effect of aryloxyphenoxypropionates (diclofop and haloxyfop) and cyclohexanediones (sethoxydim and clethodim) on root cortical cell membrane potential of graminicide-susceptible and -tolerant corn (Zea mays L.) lines. l h e graminicide-tolerant corn line contained a herbicide-insensitive form of ACCase. l h e effect of the herbicides on membrane potential was similar i n both corn lines. At a concentration of 50 p~, the cyclohexanediones had little or no effect on the membrane potential of root cells. At pH 6, 50 p~ diclofop, but not haloxyfop, depolarized membrane potential, whereas both herbicides (50 p~) dramatically depolarized membrane potential at pH 5. Repolarization of membrane potential after remova1 of haloxyfop and diclofop from the treatment solution was incomplete at pH 5. However, at pH 6 nearly complete repolarization of membrane potential occurred after removal of diclofop. In graminicide-susceptible corn, root growth was significantly inhibited by a 24-h exposure to 1 p~ haloxyfop or sethoxydim, but cell membrane potential was unaffected. In gramincidetolerant corn, sethoxydim treatment (1 p~, 48 h) had no effect on root growth, whereas haloxyfop (1 IM, 48 h) inhibited root growth by 78%. However, membrane potential was the same in roots treated with 1 p~ haloxyfop or sethoxydim. l h e results of this study indicate that graminicide tolerance in the corn line used i n this investigation is not related to an altered response at the cell membrane level as has been demonstrated with other resistant species.Aryloxyphenoxypropionate (haloxyfop and diclofop3) and cyclohexanedione (sethoxydim and clethodim) herbicides, referred to as graminicides, are used to coritrol grass weeds in certain dicotyledonous and small grain crops (Humburg et al., 1989). There is strong evidence that the target site of these herbicides in sensitive grass species is ACCase (EC 6.4.1.2), a plastid-localized enzyme that catalyzes the ATPdependent carboxylation of acetyl-COA to form malonyl-COA (Hoppe and Zacher, 1985;Burton et al., 1987;Focke and Lichtenthaler, 1987; Rendina and Felts, 1988;Secor and Cséke, 1988). By inhibiting ACCase of sensitive grasses, the graminicides prevent de novo fatty acid biosynthesis and thereby block fatty acid production. Resistance to the aryloxyphenoxypropionates and cyclohexanediones in dicots is due to the presence of a herbicide-insensitive form of ACCase (Burton et al., 1989). Some grasses (e.g. wheat) are tolerant to these herbicides because they can metabolize them (Shimabukuro, 1990). Other grasses are resistant because they contain a resistant form of ACCase. Diclofop resistance in a Lolium multiflorum biotype selected under field conditions is due to the presence of a resistant form of ACCase Gronwald et al., 1992). Furthermore, in c...