<p>Tannic acid (TA), a naturally occurring polyphenol, exhibits broad-spectrum antimicrobial and antioxidant activities. This study elucidates the mechanisms by which TA controls <i>Alternaria alternata</i> in Korla fragrant pears. In vitro, TA at 10 mg mL<sup>−</sup><sup>1</sup> 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.</p><p></p>

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

  • Yisong Tang,
  • Weida Zhang,
  • Wanting Yang,
  • Tongrui Sun,
  • Jiankang Cao,
  • Shaobo Cheng,
  • Guogang Chen

摘要

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 mL1 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.