β-Aminobutyric Acid Alleviates Chilling Injury in Postharvest Apricot Fruit by Regulating Membrane Lipid Metabolism and Reactive Oxygen Species Scavenging

Chilling injury (CI) is a major postharvest disorder that limits the storage life of apricot fruit. In this study, the effects of β-aminobutyric acid (BABA) on CI development, membrane lipid metabolism, and reactive oxygen species metabolism in apricot fruit were investigated. “Shushanggan” apricots were treated with 20 mM BABA and stored at 1 °C for 42 d. Results showed that BABA treatment significantly reduced the CI index, maintained higher fruit firmness, and delayed the respiratory peak compared to the control fruit. BABA suppressed the activities of phospholipase D, lipase, and lipoxygenase, which resulted in higher retention of phosphatidylcholine and phosphatidylinositol, lower accumulation of phosphatidic acid, and higher unsaturated fatty acid contents. BABA-treated fruit also exhibited lower superoxide anion production rate, hydrogen peroxide content, hydroxyl radical content, and malondialdehyde accumulation. In addition, BABA enhanced the activities of superoxide dismutase, catalase, and ascorbate peroxidase, maintained higher levels of ascorbate and glutathione, and increased DPPH radical scavenging rate and total reducing power. These findings indicate that BABA alleviates CI in apricot fruit by regulating membrane lipid metabolism and ROS metabolism and suggest that BABA treatment could be a useful strategy for reducing postharvest losses of apricot fruit during cold storage.

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