Exogenous nitric oxide treatment regulates ROS metabolism and delays the postharvest lignification of loquat fruit during cold storage

To investigate the regulatory effects of nitric oxide (NO) on reactive oxygen metabolism in postharvest loquat fruit and its association with chilling injury (CI) and storability, we conducted a study using cv. "Jiefangzhong" loquat fruit. The fruit was fumigated with 20 mu L<middle dot>L- 1 NO gas and stored at 4 +/- 1 degrees C with 85%+/- 5% relative humidity. Throughout the storage period, samples were taken to assess lignification and the dynamics of reactive oxygen species (ROS) production and scavenging. The results demonstrated that NO-treated loquat fruit exhibited significantly higher fruit firmness and extractable juice rate, along with lower cell membrane permeability and malondialdehyde content compared to the control group. Notably, the CI index and lignin content were reduced by approximately 8% and 42%, respectively. Furthermore, NO treatment significantly decreased the superoxide anion production rate and hydrogen peroxide content, while enhancing the activities of superoxide dismutase, catalase, and ascorbate peroxidase. It also inhibited peroxidase activity. Additionally, NO treatment increased the levels of ascorbic acid and reduced glutathione (GSH), boosted the activities of monodehydroascorbate reductase, dehydroascorbate reductase, and GSH reductase, and significantly reduced the contents of dehydroascorbic acid and oxidized GSH (GSSG). These changes contributed to a higher total antioxidant capacity in the NO-treated fruit compared to the control. These findings indicate that NO treatment can mitigate the lignification of loquat fruit during low-temperature storage. This effect is likely due to the enhancement of ROS-scavenging systems by NO leading to reduced ROS levels and oxidative stress, and thereby inhibiting the CI-induced physiological disorder associated with.