Abstract
The herbicide bromoxynil (3,5-dibromo-4-hydroxybenzonitrile) was tested on mitochondria from etiolated pea (Pisum sativum L. cv Alaska) stems. This compound when used at micromolar concentrations ([almost equal to]20 [mu]M) inhibited malate- and succinate-dependent respiration by intact mitochondria but not oxidation of exogenously added NADH. Bromoxynil did not affect the activities of the succinic and the internal NADH dehydrogenases. Analyses of the effects induced by this herbicide on the membrane potential, [delta]pH, matrix Ca2+ movements, and dicarboxylate transport demonstrated that bromoxynil is likely to act as an inhibitor of the dicarboxylate carrier. In addition, bromoxynil caused a mild membrane uncoupling at concentrations [greater than or equal to]20 [mu]M. No effect on the ATPase activity was observed.
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