An investigation into the role of lipid peroxidation in the mode of action of aromatic hydrocarbon and dicarboximide fungicides

Abstract

The mode of actio of aromatic hydrocarbon and dicarboximide fungicides has been the subject of many studies which have not conclusively identified the primary target site. One current theory proposes that active oxygen species generated by these compounds initiate lipid peroxidation. We studied the effects of two aromatic hydrocarbons, chloroneb and tolclophos-methyl, and three dicarboximides, vinclozolin, iprodione, and myclozoline, on microsomes of Ustilago maydis. As a control, we compared the effect of paraquat, which is known to generate active oxygen, with that of these fungicides. Growth of U. maydis is very sensitive to all five compounds under study, especially to tolchlophos-methyl (I 50 = 0.3 μg/ml). No lipid peroxidation occurred in the fungal microsomes when treated with the fungicides. In fact, no peroxidation was observed when the fungal microsomes were treated with a potent oxidation system of ascorbate iron. This may be explained by the lack of highly polyunsaturated fatty acids in this fungus. Whereas paraquat caused the uncoupling of electron flow in U. maydis microsomes as demonstrated by NADPH oxidation and O 2 consumption, no effect was observed upon treatment with the fungicides. These compounds also did not inhibit NADPH-cytochrome P450 reductase activity. These results suggest that lipid peroxidation as the primary mode of action of these compounds is unlikely in this organism.