Postharvest browning and senescence significantly reduce the commercial value of litchi, a nutritious tropical fruit. Although itaconate, a branched-chain metabolite of the tricarboxylic acid (TCA) cycle, is known as a food preservative, its effects on litchi fruit deterioration remain unclear. This study demonstrates that itaconate treatment effectively delays pericarp browning and suppresses respiratory rates in litchi fruit. The treatment enhanced the antioxidant capacity by boosting the activities of superoxide dismutase, catalase, and ascorbate peroxidase, while inhibiting peroxidase and polyphenol oxidase. Consequently, hydrogen peroxide, superoxide anions, and malondialdehyde accumulation decreased, whereas glutathione, ascorbic acid, total phenols, and anthocyanin levels increased. Furthermore, itaconate-maintained cellular energy homeostasis by elevating ATP content, energy charge, and the activity of key TCA cycle enzymes, succinate dehydrogenase and malate dehydrogenase. Transcriptomic and RT-qPCR analyses confirmed the upregulation of genes related to oxidative stress and energy metabolism ( LcCAT , LcSOD , LcAPX1 , LcF3H , LcUFGT , LcAtpB ). Collectively, these findings indicate that itaconate mitigates browning and senescence in litchi fruit by improving redox balance and sustaining energy homeostasis. • Itaconate delays senescence and pericarp browning in postharvest litchi. • Itaconate upregulates genes for oxidative stress and energy metabolism in litchi. • Itaconate alleviates oxidative stress by enhancing antioxidants and suppressing ROS. • Itaconate maintains energy homeostasis by promoting TCA cycle activity.
Qin et al. (Mon,) studied this question.