Mechanism of Action of the Diphenyl Ether Herbicide Acifluorfen-Methyl in Excised Cucumber (Cucumis sativus L.) Cotyledons

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Abstract
Cucumber (C. sativus L.) cotyledons were sensitive to the diphenyl ether herbicide acifluorfen-methyl (AFM); methyl 5-[2-chloro-4-(trifluoromethyl)phenoxyl]-2-nitrobenzoate. Injury was detected by monitoring the efflux of 86Rb+ from treated tissues after exposure to light (600 micro .mu. einsteins/m2/s.; photosynthetically active radiation). AFM exhibited activity in green and etiolated tissues in the presence of 1 .mu.M 3-(3,4-dichlorophenyl)-1,1-dimethylurea (DCMU) and 1 .mu.M 2,5-dibromo-3-methyl-6-isopropyl-p-benzoquinone (DBMIB), inhibitors of photosynthetic electron transport. Protection against injury could be obtained by pretreating the seedlings with a carotenoid biosynthesis inhibitor, 10 .mu.M fluridone [1-methyl-3-phenyl-5-[3-(trifluoromethyl)phenyl]-4(H)-pyridinone]. After a 4-h dark pretreatment with 1 and 10 .mu.M AFM, cotyledons were exposed to light (600 .mu. einsteins/m2/s; photosynthetically active radiation). Within 1-2 h after light treatment, significant increases in the level of thiobarbituric acid-reacting materials could be detected. EM observations of treated tissues revealed significant structural damage to the chloroplast envelope, tonoplast and plasma membrane. Etiolated cucumber cotyledons treated with 1 .mu.M AFM and exposed to light were less susceptible to injury when maintained in an O2-deficient atmosphere. Protection against injury could be obtained with 50 .mu.M .alpha.-tocopherol. Evidently, AFM is activated in light by yellow plant pigments and then is involved in the initiation of a free radical chain reaction with polyunsaturated fatty acid moieties of phospholipid molecules making up cellular membranes. The perturbations that follow result in a loss of the membrane''s selectve permeability characteristics, thereby leading to cellular death.