Mechanism of action of the diphenyl ether herbicide acifluorfen-methyl in excised cucumber (Cucumis sativus L.) cotyledons. Light activation and the subsequent formation of lipophilic free radicals

• Published in: Plant physiology (Bethesda) Vol. 69; no. 2; pp. 502 - 507
• Main Authors: Orr, G.L, Hess, F.D
• Format: Journal Article
• Language: English
• Published: United States American Society of Plant Physiologists 01.02.1982
• Subjects: Carotenoids; Cell membranes; Cotyledons; Cucumbers; Ethanol; Ethers; Free radicals; Herbicides; Lipid peroxides; Unsaturated fatty acids
• ISSN: 0032-0889; 1532-2548
• DOI: 10.1104/pp.69.2.502

Cucumber (Cucumis sativus L.) cotyledons were sensitive to the diphenyl ether herbicide acifluorfen-methyl (AFM); methyl 5-[2-chloro-4-(trifluoromethyl)phenoxy]-2-nitrobenzoate. Injury was detected by monitoring the efflux of 86Rb+ from treated tissues after exposure to light (600 micro einsteins per $\text{meter}^{2}$ per second; photosynthetically active radiation). AFM exhibited activity in green and etiolated tissues in the presence of both 1 micromolar 3-(3,4-dichlorophenyl)-1,1-dimethylurea (DCMU) and 1 micromolar 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 micromolar fluridone {1-methyl-3-phenyl-5-[3-(trifluoromethyl)phenyl]-4(H)-pyridinone}. After a 4-hour dark pretreatment with 1 and 10 micromolar AFM, cotyledons were exposed to light (600 micro einsteins per $\text{meter}^{2}$ per second; photosynthetically active radiation). Within 1 to 2 hours after light treatment, significant increases in the level of thiobarbituric acid-reacting materials could be detected. Electron microscopic observations of treated tissues revealed significant structural damage to the chloroplast envelope, tonoplast, and plasma membrane. Etiolated cucumber cotyledons treated with 1 micromolar 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 micromolar α-tocopherol. These results suggest 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 selective permeability characteristics, thereby leading to cellular death.