Enzymatic tissue browning caused by biological membrane degradation in the young immature fruit of 'Moriya' persimmon (Diospyros kaki Thunb.).

• Browning of young 'Moriya' persimmon involves biological membrane degradation. • PPO, POD and polyphenols eluted from the damaged membrane and react in the cytoplasm. • Increased expressions of DkPLDs and DkLOX3 affected membrane degradation. • Ascorbic acid's antioxidant activity may curb PPO and POD's phenolic oxidation. Determining the mechanism of fruit tissue browning is important to prevent fruit quality degradation and reduce fruit loss at the postharvest stage in persimmons. We aimed to provide a fundamental understanding of the mechanism of browning of mature persimmon fruit and contribute to develop a method for its prevention over the course of the marketing supply chain by analyzing the browning of young immature persimmon fruit. Tissue browning was first observed seven days after harvest (DAH), and spontaneous ethylene production was initiated at five DAH. The activities of the browning enzymes polyphenol oxidase (PPO) and peroxidase (POD) were sufficiently high to induce fruit tissue browning. As these enzymes are normally sequestered by biological membranes in cells, we hypothesized that biological membrane degradation occurs prior to browning. Electrolyte leakage and the increase in malondialdehyde content occurred during storage. An increase in malondialdehyde content provided evidence of progressive membrane degradation. The increased expression of phospholipase relative DkPLD alpha1, DkPLD beta/gamma1 , and lipoxygenase relative DkLOX3 genes, probably induced by ethylene, indicated their significant roles in membrane degradation. The ascorbic acid may play a role in inhibiting the oxidation of phenolic substrates by PPO and POD owing to its antioxidant activity. The results of our study suggest that the hydrolysis of phospholipids by DkPLD alpha1 and DkPLD beta/gamma1 and peroxidation by DkLOX3 promote biological membrane degradation in both persimmon skin and flesh. Additionally, we hypothesized that the decrease in L-ascorbic acid content could induce browning, as a result of PPO and POD leaked from the biological membrane could react with phenolic substrates. [ABSTRACT FROM AUTHOR]