Exogenous deferoxamine mesylate suppresses iron-dependent ferroptosis in postharvest fruit rot of blueberry caused by Alternaria alternata and Fusarium fujikuroi

Plant development relies heavily on regulated cell death, which is crucial for specific plant responses to biological stresses. Ferroptosis, an iron-dependent, oxidative, and non-apoptotic cell death form, has been recently discovered in animal cells. In this study, we investigated whether a ferroptosis-like process could be relevant to cell death in postharvest fruit rot of blueberry caused by Alternaria alternata and Fusarium fujikuroi. The results showed that deferoxamine mesylate and glutathione (GSH) treated fruit showed enhanced disease resistance with lower lesion areas, whereas an opposite result was observed in hydrogen peroxide (H₂O₂) treatment, indicating that intracellular ferroptosis might exist in the fungal infected blueberry fruit. Compared to control, deferoxamine mesylate or GSH treatment improved chlorophyll fluorescence parameters, which contributed to the stability of photosynthesis. In terms of ferroptosis pathway in the adjacent area of infected fruit, deferoxamine mesylate suppressed an iron-dependent cell death pathway that was characterized by depletion of H₂O₂ and MDA and accumulation of GSH, as well as the reduction of ferrous ions and total iron ions. Meanwhile, deferoxamine mesylate could effectively delay the decrease rate of unsaturation value and key phospholipids of fungi infected fruit during storage, which possibly maintained the integrity of cell membrane. Due to the serious rot of the lesion area, the peroxidation of membrane lipids was severe, accompanied by metabolic disorders. These combined results demonstrated that deferoxamine mesylate treatment could reduce Fenton reaction by chelating Fe²⁺ and avoid excessive accumulation of reactive oxygen species (ROS), suppress iron-dependent ferroptosis, thereby maintaining fruit quality and reducing postharvest diseases.