Abstract
The herbicide dicamba (3,6‐dichloro‐2‐methoxybenzoic acid) was evaluated for its effects on bioenergetic activities of potato tuber mitochondria to elucidate putative mechanisms of action and to compare its toxicity with 2‐chlorobenzoic acid. Dicamba (4 μmol/mg mitochondrial protein) induces a limited stimulation of state 4 respiration of ca. 10%, and the above concentrations significantly inhibit respiration, whereas 2‐chlorobenzoic acid maximally stimulates state 4 respiration (ca. 50%) at about 25 μmol/mg mitochondrial protein. As opposed to these limited effects on state 4 respiration, transmembrane electrical potential is strongly decreased by dicamba and 2‐chlorobenzoic acid. Dicamba (25 μmol/mg mitochondrial protein) collapses, almost completely, Δψ; similar concentrations of 2‐chlorobenzoic acid promote Δψ drops of about 50%. Proton permeabilization partially contributes to Δψ collapse since swelling in K‐acetate medium is stimulated, with dicamba promoting a stronger stimulation. The Δψ decrease induced by dicamba is not exclusively the result of a stimulation on the proton leak through the mitochondrial inner membrane, since there was no correspondence between the Δψ decrease and the change on the O~2~ consumption on state 4 respiration; on the contrary, for concentrations above 8 μmol/mg mitochondrial protein a strong inhibition was observed. Both compounds inhibit the activity of respiratory complexes II and III but complex IV is not significantly affected. Complex I seems to be sensitive to these xenobiotics. In conclusion, dicamba is a stronger mitochondrial respiratory chain inhibitor and uncoupler as compared to 2‐chlorobenzoic acid. Apparently, the differences in the lipophilicity are related to the different activities on mitochondrial bioenergetics. © 2003 Wiley Periodicals, Inc. J Biochem Mol Toxicol 17:185–192, 2003; Published online in Wiley InterScience (www.interscience.wiley.com). DOI 10.1002/jbt.10077