Alpha-ketoglutaric acid alleviates litchi fruit browning and senescence via enhancing antioxidant capacity and energy homeostasis

AKG treatment delays postharvest senescence and pericarp browning in litchi fruit. • AKG upregulates genes linked to oxidative stress defense and energy metabolism. • AKG mitigates oxidative stress via enhanced antioxidant activity and reduced ROS accumulation. • AKG sustains energy homeostasis by activating TCA cycle flux. Litchi fruit are highly susceptible to browning during ambient storage, which results in a marked reduction in commercial value. This study investigated the regulatory effects and underlying mechanisms of α-ketoglutaric acid (AKG) on postharvest browning and senescence in litchi fruit. AKG treatment significantly reduced the browning index, delayed pigment degradation, and preserved cell membrane integrity. Moreover, AKG treatment alleviated the accumulation of reactive oxygen species (ROS) and enhanced antioxidant capacity. In parallel, AKG elevated the activities of key enzymes involved in the tricarboxylic acid (TCA) cycle, maintained high ATP levels and energy charge, and thereby provided sufficient energy to support ROS scavenging and cellular repair processes. Consequently, AKG synergistically improved both antioxidant capacity and energy metabolism. Transcriptomic analysis further revealed that AKG modulated the expression of genes associated with oxidoreductase activity, transmembrane transporter function, glycosyltransferase activity, and organic acid transmembrane transporter activity. Specifically, AKG downregulated genes involved in browning and lignin synthesis ( LcGOLS2 , Lc4CL3 , LcLAC14 ), ethylene signaling regulators ( LcEIN4 , LcERF4 , LcERS1 ), and senescence regulators ( LcNAC083 , LcNAC090 , LcNAC100 , LcWRKY75 , LcMYB73 ), while upregulating stress-responsive genes ( LcTIFY9 , LcbZIP44 and LcbHLH123 ). Collectively, these findings demonstrate that AKG delays postharvest browning and senescence in litchi by modulating ROS metabolism, enhancing TCA cycle-mediated energy production, and suppressing the expression of senescence-related genes.