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Plant and Cell Physiology, 1986, Vol. 27, No. 1 11-15
© 1986

Article

Acifluorfen and Oxidized Ubiquinone in Soybean Mitochondria

Robert E. Hoagland1, Deborah J. Hunter2 and Marvin L. Salin2

1Southern Weed Science Laboratory USDA, ARS, P.O. Box 225, Stoneville, MS 38776, U.S.A.
2Department of Biochemistry, Mississippi State University Mississippi State, MS 39762, U.S.A.

Intact mitochondria from soybean [Glycine max (L.) Merrill cv Bragg] seedlings were incubated with acifluorfen {sodium-5-[2-chloro-4-(trifluoromethyl)phenoxy]-2- nitrobenzoate}. Respiration, measured as O2 consumption, was inhibited by acifluorfen with a 50% inhibition occurring with 10 µM of the herbicide. The inhibition was unaffected by illumination; moreover, prior illumination by either UV or visible light did not alter the inhibition capacity of acifluorfen. Further examination of the locus of acifluorfen inhibition at the electron transport chain level showed no inhibition in Cyt c oxidation capacity as well as no effect on NADH dehydrogenase, succinate dehydrogenase, malate dehydrogenase and isocitrate dehydrogenase. It was observed, however, that in mitochondria incubated for 10 min with 0.2 µM acifluorfen, ubiquinone existed predominantly in the oxidized state. We conclude that at the mitochondrial level, a possible major site of action of acifluorfen is either a direct or indirect modulation of the redox potential of ubiquinone.

(Received July 27, 1985; Accepted October 7, 1985)
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