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Environmental and Stress Physiology

Mode of Action Studies on Nitrodiphenyl Ether Herbicides

I. Use of Barley Mutants to Probe the Role of Photosynthetic Electron Transport

Department of Biochemistry, Royal Holloway and Bedford New College, Egham Hill, Egham, Surrey TW20 OEX, United Kingdom, Shell Research Limited, Sittingbourne Research Centre, Sittingbourne, Kent ME9 8AG, United Kingdom

5-[2-Chloro-4-(trifluoromethyl)phenoxy]-2-nitroacetophenone oxime-o-(acetic acid, methyl ester) (DPEI), is a potent nitrodiphenyl ether herbicide which causes rapid leaf wilting, membrane lipid peroxidation, and chlorophyll destruction in a process which is both light- and O₂-dependent. These effects resemble those of other nitrodiphenyl ether herbicides. Unlike paraquat, the herbicidal effects of DPEI are only slightly reduced by pretreatment with the photosynthetic electron transport inhibitor 3-(3,4-dichlorophenyl)-1,1-dimethylurea. DPEI is a weak inhibitor of photosynthetic electron transport (I₅₀ 15 micromolar for water to paraquat) in vitro, with at least one site of action at the cytochrome b₆f complex. Ultrastructural studies and measurements of ethane formation resulting from lipid peroxidation indicate that mutants of barley lacking photosystem I (PSI) (viridis-zb⁶³) or photosystem II (viridis-zd⁶⁹) are resistant to paraquat but susceptible to DPEI. The results indicate that electron transfer through both photosystems is not essential for the toxic effects of nitrodiphenyl ether herbicides. Furthermore, the results show that neither cyclic electron transport around PSI, nor the diversion of electrons from PSI to O₂ when NADPH consumption is blocked are essential for the phytotoxicity of nitrodiphenyl ether herbicides.