Acifluorfen and Oxidized Ubiquinone in Soybean Mitochondria

Intact mitochondria from soybean Glycine max (L.) Merrill cvBragg] seedlings were incubated with acifluorfen {sodium-5-2-chloro-4-(trifluoromethyl)phenoxy]-2-nitrobenzoate}. Respiration, measured as O₂ consumption, wasinhibited by acifluorfen with a 50% inhibition occurring with10 µM of the herbicide. The inhibition was unaffectedby illumination; moreover, prior illumination by either UV orvisible light did not alter the inhibition capacity of acifluorfen.Further examination of the locus of acifluorfen inhibition atthe electron transport chain level showed no inhibition in Cytc oxidation capacity as well as no effect on NADH dehydrogenase,succinate dehydrogenase, malate dehydrogenase and isocitratedehydrogenase. It was observed, however, that in mitochondriaincubated for 10 min with 0.2 µM acifluorfen, ubiquinoneexisted predominantly in the oxidized state. We conclude thatat the mitochondrial level, a possible major site of actionof acifluorfen is either a direct or indirect modulation ofthe redox potential of ubiquinone. (Received July 27, 1985; Accepted October 7, 1985)