Energy and respiratory metabolism participate in dicyclohexylcarbodiimide and disodium succinate-mediated the alteration of energy status modulating pericarp browning of fresh longan.

Pericarp browning is a major symptom of the quality deterioration in postharvest longan fruit. Previous studies show that the change in the quality of fresh produce is related to the level of energy status. The proton transport regulator such as dicyclohexylcarbodiimide (DCC) and disodium succinate (DS) can regulate the protons flux to affect the production of adenosine triphosphate (ATP) and the level of energy status. However, the mechanisms of proton transport regulator induced-the changes in the level of ATP and energy status in postharvest longan fruit in relation to longan pericarp browning remain unclear. In this work, the influences of DCC and DS-mediated the alteration of energy status on longan pericarp browning, energy metabolism, and respiratory metabolism were investigated. Results showed that DCC treatment accelerated pericarp browning development and elevated respiration rate as compared to the control. Longans treated with DCC exhibited higher levels of ATP, adenosine diphosphate (ADP), and energy charge, as well as higher activities of H+-ATPase, Ca2+-ATPase, and Mg2+-ATPase in the mitochondrial, vacuole, and plasma membranes. Additionally, DCC treatment increased the activities of phosphoglucose isomerase (PGI), succinate dehydrogenase (SDH), cytochrome C oxidase (CCO), ascorbic acid oxidase (AAO), and alternative oxidase (AOX), along with higher contents of ubiquinol (QH 2), nicotinamide adenine dinucleotide (NAD), and the reduced form of NAD (NADH). Whereas, DCC treatment decreased the activities of nicotinamide adenine dinucleotide kinase (NADK), and glucose-6-phosphate dehydrogenase (G-6-PDH) + 6-phosphaogluconate dehydrogenase (6-PGDH), and lowered the contents of ubiquinone (Q), nicotinamide adenine dinucleotide phosphate (NADP), and the reduced form of NADP (NADPH). These results revealed that DCC treatment accelerated energy deficit, disrupted energy balance, and promoted respiratory metabolism through enhancing embden-meyerhof-parnas (EMP), tricarboxylic acid (TCA) cycle, and cytochrome pathway (CCP) while attenuating pentose phosphate pathway (PPP), ultimately leading to the aggravated longan pericarp browning. Conversely, DS treatment delayed longan pericarp browning by acting on the opposite effects of DCC treatment. • DCC hastened longan pericarp browning, whereas DS had the opposite effect. • DCC lowered energy status of longan pericarp, but DS retained a higher energy status. • DCC reduced ATPase activities in longan pericarp, but DS enhanced these activities. • DCC raised EMP-TCA cycle and CCP, but reduced PPP, DS exhibited the opposite pattern. • DCC speeded energy deficit and respiratory metabolism, but DS retarded this process. [ABSTRACT FROM AUTHOR]