Spermidine treatment delays postharvest senescence of prune (Prunus domestica L.) fruit by regulating reactive oxygen species and membrane lipid metabolism

Abstract

Spermidine (Spd), a membrane stabilizer and free radical scavenger, plays a pivotal role in delaying post-harvest fruit senescence. Herein, prune fruit was treated with Spd to explore its impact on fruit quality, with D-arginine (D-arg), a polyamine inhibitor, utilized as a negative control. We focused on analyzing the regulatory effects of both treatments on reactive oxygen species (ROS) and membrane lipid metabolism in prune fruit. The results showed that Spd reduced respiration rate and weight loss while maintaining high levels of firmness, soluble solid content (SSC), and titratable acid (TA). Spd maintained elevated levels of ascorbic acid (AsA) and glutathione (GSH), enhanced ROS scavenging enzyme activities and antioxidant capacity, thereby mitigating ROS-induced oxidative damage to cell membranes. Moreover, Spd inhibited the activities of phospholipid-degrading enzymes while sustaining elevated fatty acid desaturase (FADS) activity. Thus, Spd increased the levels of phosphatidylcholine (PC), phosphatidylinositol (PI), unsaturated fatty acids (USFAs), unsaturated fatty acid index (IUFA), and the ratio of unsaturated fatty acids to saturated fatty acids (U/S). Concurrently, Spd inhibited the accumulation of oxidative stress products and saturated fatty acids (SFAs), mitigated the increase in cell membrane permeability (CMP), thereby sustaining the structural and morphological integrity of mitochondria and cellular membranes in prune fruit. In contrast, D-arg treatment yielded diametrically opposite results. These results indicate that Spd delays prune fruit senescence by regulating ROS and membrane lipid metabolism.