Investigating the Antifungal Mechanism of Hinokitiol Against : Inducing Oxidative Damage to Membrane System, Cell Wall Structure and Mitochondrial Function.

Citrus sour rot is normally caused by , which not only deteriorates fruit quality but also causes huge economic losses annually. The current study delves into the underlying in vitro antifungal mechanisms of hinokitiol and assesses its efficacy in controlling sour rot development on navel oranges infected by . Both in vitro and in vivo examinations demonstrate that hinokitiol exhibits strong antifungal activity against , with a minimum inhibitory concentration and minimum fungicidal concentration of 25.0 mg/L, resulting in a significant reduction in citrus sour rot disease. Decreased blue fluorescence in CFW staining and cell wall components have confirmed that hinokitiol disrupts the structural organization of the cell wall. Additionally, hinokitiol induces abnormal mycelial growth, causing more severe deformities, dried blights, plasmalemma wall separation, mitochondrial decomposition, and cell permeabilization. Furthermore, hinokitiol increases the production of HO, O and MDA levels in , resulting in permanent damage to cell membrane integrity, mitochondrial oxidative phosphorylation, and DNA function, ultimately triggering cell apoptosis. These results indicate that hinokitiol is a novel antifungal agent for controlling postharvest sour rot in citrus fruits. This study contributes new insights into the control of postharvest fungal decay and elucidates hinokitiol's antifungal mechanism against .