Lipid Peroxidation and Membrane Disruption by Vinclozolin in Dicarboximide-Susceptible and -Resistant Isolates ofBotrytis cinerea

Abstract

A dicarboximide-susceptible (DS) isolate and a dicarboximide-resistant (DR) isolate ofBotrytis cinereawere compared with regard to spore germination, mycelial growth, cellular leakage, and lipid peroxidation upon treatment with the dicarboximide fungicide vinclozolin. The fungicide inhibited spore germination and mycelial growth of the DS isolate, but not those of the DR isolate. The inhibitory effect of the fungicide was greater on mycelial growth than on spore germination of the DS isolate. Significant cellular leakage from the fungicide-treated DS or DR isolate began to increase after 24 hr incubation, depending on the concentration of the fungicide and the duration of incubation time. However, the magnitude of cellular leakage was much greater from the DS isolate than from the DR isolate. Vinclozolin caused considerable lipid peroxidation in the DS isolate, whereas little or no lipid peroxidation occurred in the DR isolate treated with the fungicide. Lipid peroxidation preceded cellular leakage from the DS isolate following fungicide treatment. The effects of the fungicide on mycelial growth, cellular leakage, and lipid peroxidation of the DS isolate were all reversed by the addition of α-tocopherol to the incubation medium. These results demonstrate that vinclozolin causes significant lipid peroxidation and subsequent cellular leakage from a DS isolate, but not from a DR isolate. Furthermore, they suggest that the mechanism of action of dicarboximide fungicides is associated with membrane lipid peroxidation.