ENANTIOMERS OF DICLOFOP-METHYL AND THEIR ROLE IN HERBICIDE MECHANISM OF ACTION

The effects of the enantiomers R(+) and S(-)diclofop and cerulenin, an inhibitor of fatty acid biosynthesis, on root growth, absorption of [C-14]acetate, its incorporation into cellular lipids, and changes to lipid components in susceptible oat roots indicate that the in vivo inhibition of acetyl-CoA carboxylase and lipid biosynthesis may not be the primary mechanism of action of diclofopmethyl. Tissue responses to diclofop were not due to selective uptake of enantiomers, molecular inversion, or metabolism and detoxification of the herbicide. Both enantiomers depolarized membrane potential of oat cells, resulting in reduced uptake of [C-14]acetate but its in vivo incorporation into cellular lipids was unaffected. Cerulenin was most effective in inhibiting lipid biosynthesis in vivo. However, oat root growth was inhibited significantly by R(+)diclofop but only slightly by cerulenin and S(-)diclofop. Both enantiomers and cerulenin caused lipid profile changes with decreased levels of phospholipids in oat root tips relative to control within 3 hr. Cerulenin may cause a decrease in phospholipid biosynthesis by limiting the levels of free fatty acids as substrates, but this does not appear to be the mechanism for R(+) and S(-)diclofop. The role of oxidative membrane catabolism by free radical lipid peroxidation and its coupling to the effect of diclofop on the transmembrane proton gradient are discussed as the most likely mechanism of action of diclofopmethyl. The proposed mechanism explains the reversal of phytotoxicity by auxinic herbicides, lipoxygenase inhibitors, and free radical scavengers. (C) 1995 Academic Press, Inc.