The effect of diclofop on membrane potential, ethylene induction, and herbicide phytotoxicity in resistant and susceptible biotypes of grasses

Diclofop-methyl (DM) and haloxyfop-ethoxyethyl (HE) are effective inducers of ethylene in susceptible species. Ethylene is a collateral product result ing from oxidative stress due to the production of reactive oxygen species (ROS). Lipoxygenase (LOX) inhibitors, free radical scavengers, and 2,4-D re verse the phytotoxicity of HE and DM, respectively, by interrupting the for mation or action of ROS as indicated by the inhibition of ethylene induced by HE and DM. DM caused irreversible damage to apical meristems in suscepti ble biotypes of Lolium rigidum, Alopecurus myosuroides, and Lolium multiflo rum at 10 mM DM within 22-24 h after treatment (HAT). Damage to apical meri stems was indicated by the extent of new shoot regrowth from excised stems of the monocots. The apical meristems of all resistant biotypes of the thre e species were relatively unaffected. DM increased ethylene evolution withi n 22-24 HAT in susceptible biotypes of L. rigidum, A. myosuroides, and L. m ultiflorum (177, 224, and 155% of control, at 5, 10, and 15 mM DM, respecti vely). Little or no increase in ethylene formation above their controls was induced by DM in any of the resistant biotypes. The membrane potentials (E -m) of susceptible L. rigidum and L. multiflorum were depolarized by 10 mu M diclofop whereas depolarization of susceptible A. myosuroides required 25 mu M diclofop. Repolarization of E-m did not occur in all susceptible biot ypes upon removal of diclofop. The E-m of all resistant biotypes was unaffe cted at 10 mu M diclofop but, except for L.. rigidum (R1), depolarization o f E-m occurred at 25 mu M diclofop. However, in contrast to the susceptible biotypes, repolarization of E-m occurred in the resistant biotypes upon re moval of exogenous diclofop. The correlation among injury to apical meriste m tissues, ethylene induction, and response of E-m to diclofop was consiste nt with the resistance or susceptibility of the biotypes to DM. Oxidative s tress resulting in the formation of ROS is the most likely lethal mechanism of action of DM. (C) 1999 Academic Press.