Comparative effects of herbicide dicamba and related compound on plant mitochondrial bioenergetics

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 mol/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 mol/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 mol/mg mitochondrial protein) collapses, almost completely, ∆ψ; similar concentrations of 2-chlorobenzoic acid promote ∆ψ drops of about 50%. Proton permeabilization partially contributes to ∆ψ collapse since swelling in Kacetate medium is stimulated, with dicamba promoting a stronger stimulation. The ∆ψ 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 ∆ψ decrease and the change on the O 2 consumption on state 4 respiration; on the contrary, for concentrations above 8 mol/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.

Health and Cellular Impacts of Air Pollutants: From Cytoprotection to Cytotoxicity

“…Through all examples cited previously, it is clear that cytotoxicity of air pollutants (PM, PAHs, metals, or herbicides) in various cells [70, 78, 133] mainly incriminates the excessive production of ROS capable of targeting mitochondria by different mechanisms (Figure 1) [83, 134]. At the same time as the ROS-dependent apoptosis, some other oxidative stress-independent signaling pathways have been identified.…”

Herbicides: the Face and the Reverse of the Coin. An in Vitro Approach to the Toxicity of Herbicides in Non-Target Organisms

“…From these results it was concluded that dicamba decreases oxidative phosphorylation by a dual effect on the redox chain (inhibition of redox complexes, and stimulation of proton leakage through the mitochondrial inner membrane) (Peixoto et al, 2003a). Similarly to rat liver mitochondria, dicamba interfered with potato tuber mitochondria by inhibiting the activities of the respiratory complexes II and III, of ATP synthase, and also stimulating the proton leakage through the mitochondrial inner membrane (Peixoto et al, 2003b). In turn, comparative effects of dicamba and a related compound, 2-chlorobenzoic acid, on potato tuber mitochondria showed that dicamba is a stronger mitochondrial respiratory chain inhibitor and uncoupler.…”

“…In turn, comparative effects of dicamba and a related compound, 2-chlorobenzoic acid, on potato tuber mitochondria showed that dicamba is a stronger mitochondrial respiratory chain inhibitor and uncoupler. So, considering the results, it was suggested that differences in the lipophilicity due to their chemical structures are related to the different sensitivities of mitochondrial bioenergetics to the referred compounds (Peixoto et al, 2003b).…”