The chestnut postharvest pathogen Neofusicoccum parvum (N. parvum) is an important postharvest pathogen that causes chestnut rot. Chestnut rot in postharvest reduces food quality and causes huge economic losses. This study aimed to evaluate the inhibitory effect of dill seed essential oil (DSEO) on N. parvum and its mechanism of action. The chemical characterization of DSEO by gas chromatography/mass spectrometry (GC/MS) showed that the main components of DSEO were apiole, carvone, dihydrocarvone, and limonene. DSEO inhibited the growth of mycelium in a dose-dependent manner. The antifungal effects are associated with destroying the fungal cell wall (cytoskeleton) and cell membrane. In addition, DSEO can induce oxidative damage and intracellular redox imbalance to damage cell function. Transcriptomics analysis showed DSEO treatment induced differently expressed genes most related to replication, transcription, translation, and lipid, DNA metabolic process. Furthermore, in vivo experiments showed that DSEO and DSEO emulsion can inhibit the growth of fungi and prolong the storage period of chestnuts. These results suggest that DSEO can be used as a potential antifungal preservative in food storage.

This research aimed to investigate natamycin’s antifungal effect and its mechanism against the chestnut pathogen Neofusicoccum parvum. Natamycin’s inhibitory effects on N. parvum were investigated using a drug-containing plate culture method and an in vivo assay in chestnuts and shell buckets. The antifungal mechanism of action of natamycin on N. parvum was investigated by conducting staining experiments of the fungal cell wall and cell membrane. Natamycin had a minimum inhibitory concentration (MIC) of 100 μg/mL and a minimum fungicidal concentration (MFC) of 200 μg/mL against N. parvum. At five times the MFC, natamycin had a strong antifungal effect on chestnuts in vivo, and it effectively reduced morbidity and extended the storage period. The cell membrane was the primary target of natamycin action against N. parvum. Natamycin inhibits ergosterol synthesis, disrupts cell membranes, and causes intracellular protein, nucleic acid, and other macromolecule leakages. Furthermore, natamycin can cause oxidative damage to the fungus, as evidenced by decreased superoxide dismutase and catalase enzyme activity. Natamycin exerts a strong antifungal effect on the pathogenic fungus N. parvum from chestnuts, mainly through the disruption of fungal cell membranes.