The Effect of Diclofop on Membrane Potential, Ethylene Induction, and Herbicide Phytotoxicity in Resistant and Susceptible Biotypes of Grasses

Abstract

Diclofop-methyl (DM) and haloxyfop-ethoxyethyl (HE) are effective inducers of ethylene in susceptible species. Ethylene is a collateral product resulting from oxidative stress due to the production of reactive oxygen species (ROS). Lipoxygenase (LOX) inhibitors, free radical scavengers, and 2,4-D reverse the phytotoxicity of HE and DM, respectively, by interrupting the formation or action of ROS as indicated by the inhibition of ethylene induced by HE and DM. DM caused irreversible damage to apical meristems in susceptible biotypes ofLolium rigidum,Alopecurus myosuroides, andLolium multiflorumat 10 mM DM within 22–24 h after treatment (HAT). Damage to apical meristems was indicated by the extent of new shoot regrowth from excised stems of the monocots. The apical meristems of all resistant biotypes of the three species were relatively unaffected. DM increased ethylene evolution within 22–24 HAT in susceptible biotypes ofL. rigidum,A. myosuroides, andL. multiflorum(177, 224, and 155;pc of control, at 5, 10, and 15 mM DM, respectively). Little or no increase in ethylene formation above their controls was induced by DM in any of the resistant biotypes. The membrane potentials (E;zm) of susceptibleL. rigidumandL. multiflorumwere depolarized by 10 μM diclofop whereas depolarization of susceptibleA. myosuroidesrequired 25 μM diclofop. Repolarization ofEmdid not occur in all susceptible biotypes upon removal of diclofop. TheEmof all resistant biotypes was unaffected at 10 μM diclofop but, except forL. rigidum(R1), depolarization ofEmoccurred at 25 μM diclofop. However, in contrast to the susceptible biotypes, repolarization ofEμm occurred in the resistant biotypes upon removal of exogenous diclofop. The correlation among injury to apical meristem tissues, ethylene induction, and response ofEmto diclofop was consistent with the resistance or susceptibility of the biotypes to DM. Oxidative stress resulting in the formation of ROS is the most likely lethal mechanism of action of DM.