Tannic acid enhances postharvest resistance of Korla fragrant pears to Alternaria alternata by modulating membrane lipid and reactive oxygen species metabolism.

Tannic acid (TA), a naturally occurring polyphenol, exhibits broad-spectrum antimicrobial and antioxidant activities. This study elucidates the mechanisms by which TA controls Alternaria alternata in Korla fragrant pears. In vitro, TA at 10 mg mL-1 directly inhibited fungal growth by inducing hyphal deformation. In vivo, TA treatment significantly attenuated blackhead disease development. The underlying protective mechanism involved two coordinated pathways: first, TA enhanced the activity and gene expression of key antioxidant enzymes [Ascorbate peroxidase (APX), Glutathione reductase (GR), Catalase (CAT), Superoxide dismutase (SOD)], sustaining the ascorbic acid-glutathione (AsA-GSH) cycle to scavenge excessive reactive oxygen species (ROS). Second, TA suppressed the activity and gene expression of lipid-degrading enzymes [Lipoxygenase (LOX), lipase, Phospholipase C (PLC), Phospholipase D (PLD), Phospholipase A2 (PLA2)] while elevating fatty acid desaturation enzymes (FADS) activity. This regulation preserved membrane lipids [phosphatidylcholine (PC), phosphatidylinositol (PI), and unsaturated fatty acids (USFAs)], reduced harmful metabolites [phosphatidic acid (PA), free fatty acids (FFAs), and malondialdehyde (MDA)], and thereby maintained membrane integrity. Our findings demonstrate that TA functions as a multi-target postharvest treatment, primarily through the dual regulation of redox homeostasis and membrane lipid metabolism to reinforce fruit resistance.