Inhibitory effect of cinnamaldehyde on Fusarium solani and its application in postharvest preservation of sweet potato

Root rot caused by Fusarium solani is one of major postharvest diseases limiting sweet potato production. Antifungal effect and possible mode of action of cinnamaldehyde (CA) against F. solani were investigated. CA concentration of 0.075 g/L inhibited conidial viability of F. solani. CA vapor of 0.3 g/L in air completely controlled the F. solani development in sweet potatoes during storage for 10 days at 28 degrees C, and protected soluble sugar and starch in the flesh from depletion by the fungus. Further results demonstrated that CA induced reduction in mitochondrial membrane potential (Delta psi m), ROS accumulation, and cell apoptosis characterized by DNA fragmentation in F. solani. Moreover, CA facilitated decomposition of mitochondria-specific cardiolipin (CL) into its catabolites by the catalytic action of phospholipases. Altogether, the results revealed a specific antifungal mechanism of CA against F. solani, and suggest that CA holds promise as a preservative for postharvest pres-ervation of sweet potato.

Automated summary

The antifungal effect of cinnamaldehyde (CA) against Fusarium solani, a major postharvest disease in sweet potatoes, was investigated. It was found that CA inhibited the viability of F. solani and controlled its development in sweet potatoes during storage. The mechanism of action involved the reduction of mitochondrial membrane potential, accumulation of ROS, cell apoptosis, and decomposition of cardiolipin.