The systemic fungicide, flutolanil (α, α, α-trifluoro-3'-isopropoxy-o-toluanilide, Moncut^®), strongly inhibited the mycelial O₂ consumption of Rhizoctonia solani as well as the activity of succinate dehydrogenase complex (Complex II) in mitochondria, while the fungicide showed no effect on the NADH-cytochrome c reductase activity. Consequently, the site of action of flutolanil must be situated on the mitochondrial Complex II. Flutolanil was more potent in blocking the Complex II activity of R. solani than other toluanilide fungicides such as mebenil and mepronil. Neither the mycelial growth nor Complex II activity of fungi in other classes except Basidiomycetes was affected by flutolanil. Since the Complex II activity in rat liver mitochondria was also insensitive to flutolanil, a difference in enzyme susceptibility should contribute to the high selectivity in antifungal action and low mammalian toxicity of the fungicide.

This article cannot obtain the latest cited-by information.