BIOCHEMICAL-MECHANISMS INVOLVED IN SELECTIVE FUNGITOXICITY OF 2 STEROL 14-ALPHA-DEMETHYLATION INHIBITORS, PROCHLORAZ AND QUINCONAZOLE - ACCUMULATION AND METABOLISM STUDIES

The selective fungitoxic actions of prochloraz (an imidazole) and a triazole fungicide, quinconazole (3-(2,4-dichlorophenyl)-2-(1H-1,2,4-triazol-1-yl)-4(3H)-quinazolinone: II), were studied with selected phytopathogenic fungi. With the exception of Ustilago maydis, all the fungi tested were more sensitive to prochloraz than to II. A number of DMI-resistant mutants of Penicillium digitatum and P. italicum showed positive cross-resistance to both DMIs, but except for P. italicum isolate H17, the levels of resistance to II were much higher than to prochloraz. The generally higher toxicity of prochloraz to the fungi investigated, as compared to II, could not be ascribed to the slightly higher accumulation of prochloraz. With regard to prochloraz, there was no general correlation between the sensitivity of the fungi tested and the amount of fungicide accumulated. A similar situation was evident for II. However, the DMI-resistant mutants of P. italicum did show a reduced accumulation of both azoles, which may account for a low level of acquired DMI-resistance in this fungus. Since accumulation levels of the test compounds in the isolates with different degrees of resistance were the same, additional mechanisms of resistance may be involved in isolates with relatively high degrees of DMI-resistance. No detectable amounts of fungicide metabolites were found in most fungi tested over a 16-hour incubation period. Therefore, fungal metabolism is not generally responsible for the differences in sensitivity between fungi to each azole tested. It also does not generally explain the differential toxicities of prochloraz and II to each individual species. The exception to this was Rhizoctonia solani which metabolized prochloraz to a non-fungitoxic compound. This correlated with its low prochloraz sensitivity.