MECHANISM OF ACTION STUDIES ON THE DIPHENYL ETHER HERBICIDE ACIFLUORFEN-METHYL

MICHAEL PAUL ENSMINGER, Purdue University

Abstract

Cucumber (Cucumis sativus L.) cotyledons, the unicellular green alga Chlamydomonas eugametos (Moewus), and isolated spinach (Spinacia oleracea L.) chloroplast fragments were used to determine: (A) membrane disruption by diphenyl ether herbicide salts and acids, (B) the involvement of photosynthesis and free radical formation in diphenyl ether toxicity, and (C) an action spectrum for diphenyl ether herbicide toxicity. In light (600 Em('-2)s('-1)) etiolated cucumber cotyledons leaked preloaded ('86)Rb('+) after a 4 h exposure to diphenyl ether herbicides that lacked an R group or contained a salt or acid group ortho to the NO(,2) group. Cell death of C. eugametos exposed to the dephenyl ether herbicides oxyfluorfen {2-chloro-1-(3-ethoxy-4-nitrophenoxy)-4-(trifluoromethyl)benzene}, the methyl ester of acifluorfen {5-{2-chloro-4-(trifluoromethyl)phenoxy}-2-nitrobenzoic acid), and MC15608 {5-{2-chloro-4-(trifluoromethyl)phenoxy}-2-chloromethylbenzoate} required light. Acifluorfen-methyl and MC15608 toxicity decreased in an atmosphere of nitrogen and in the presence of the free radical scavengers (alpha)-tocopherol and ethanol. In most cases the toxicity of acifluorfen-methyl, oxyfluorfen, or MC15608 to C. eugametos did not decrease after simultaneous treatment with diuron {3-(3,4-dichlorophenyl)-1,1-dimethylurea}. However, diuron significantly reduced death after paraquat (1,1'-dimethyl-4,4'-bipyridinium ion) treatment at all but the highest paraquat concentration tested (1 x 10('-4)M). Isolated spinach chloroplast fragments produced malonyl dialdehyde, indicating lipid peroxidation, when paraquat or diuron was added to the medium, but no malonyl dialdehyde was produced when chloroplast fragments were treated with acifluorfen-methyl, oxyfluorfen, or MC15608. The superoxide scavenger copper penicillamine (copper complex of 2-amino-3-mercapto-3-methylbutanoic acid) eliminated paraquat activity in cucumber cotyledons but failed to protect against diphenyl ether herbicide toxicity. An action spectrum of acifluorfen-methyl revealed two peaks of light requirement; 450 and 650 to 670 nm. These data indicate that diphenyl ether herbicides which lack an R group or contain a salt or acid group ortho to the NO(,2) group on the benzene ring cause membrane disruption, acifluorfen-methyl does not directly form a free radical, and photosynthesis is not primarily required for diphenyl ether herbicide toxicity. Chlorophyll and possibly carotenoids, but not riboflavin, appear to be the pigments involved in herbicide toxicity.

Degree

Ph.D.

Subject Area

Plant sciences

COinS