Mechanism of Action and Selectivity of a Fungicide, Mepronil

Abstract

A fungicide, mepronil (3′-isopropoxy-2-methylbenzanilide, trade name: Basitac) inhibited potently the oxidation of succinate in mitochondria isolated from mycelia of Rhizoctonia solani, which was measured by oxygen consumption, while it did not affect the oxidation of NADH of mitochondria from the fungus. It inhibited the following enzymes in the isolated mitochondria from R. solani which are responsible for the oxidation of succinate; succinate-cytochrome c reductase (I₅₀: 0.25μM), succinate-coenzyme Q₁₀ reductase, succinate dehydrogenase assayed using DCPIP as an electron acceptor (I₅₀: 0.24μM, K_i: 0.082μM K_i′: 0.23μM) and succinate dehydrogenase assayed using both PMS and DCPIP as electron acceptors. It, however, did not inhibit succinate dehydrogenase which was solubilized from the mitochondria. It had no significant effect on succinate dehydrogenases in mitochondria isolated from other sources such as Pyricuralia oryzae, Botrytis cinerea, rat liver, mouse liver, etiolated pea seedling and sweet potato root. These results indicated that mepronil selectively inhibits succinate dehydrogenase in mitochondria of R. solani.