|CHENG, LAILIANG - Cornell University - New York|
|WATKINS, CHRISTOPHER - Cornell University - New York|
Submitted to: Postharvest Biology and Technology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 11/19/2011
Publication Date: 3/16/2012
Citation: Lee, J., Cheng, L., Rudell Jr, D.R., Watkins, C.B. 2012. Antioxidant metabolism of 1-methylcyclopropene (1-MCP) treated ‘Empire’ apples during controlled atmosphere storage. Postharvest Biology and Technology. 65:79-91.
Interpretive Summary: Firm flesh browning of apples is an economically cullable defect of apple fruit, especially ‘Empire’ in New York state. The disorder is characterized by moderate to severe, patterned browning of the flesh tissue and is thought to be provoked by chilling that may enhance oxidative stress. Very little is known about chemical changes that coincide with the injury or may provoke the injury. Warmer storage temperatures can be used to reduce injury but at a cost of other important fruit quality parameters such as texture and sourness. 1-MCP treatments can reduce quality at higher storage temperatures but can enhance disorder development. We measured enzyme activity and targeted metabolite linked with oxidative stress alongside untargeted metabolic profiling to link changes in apple flesh chemistry caused by conditions that both reduce and/or provoke this injury. Results indicate that enzymes related to Vitamin C metabolism may be related to disorder incidence at higher temperatures.
Technical Abstract: ‘Empire’ apples [Malus sylvestris (L.) Mill var. domestica (Borkh.) Mansf.] are susceptible to development of firm flesh browning during controlled atmosphere storage. The browning is thought to be a chilling injury and therefore fruit are typically stored at 2-3 degrees C to avoid fruit damage. However, flesh browning can be increased by 1-methylcyclopropene (1-MCP) treatment at these warmer temperatures. The objective of this work was to investigate the effect of 1-MCP on antioxidant systems of ‘Empire’ apple fruit stored at 2 kPa O2/2 kPa CO2 at either 0.5 degrees C or 3.3 degrees C for up to 40 weeks. Lightness and hue angle of flesh tissues decreased to a greater extent in 1-MCP treated than untreated fruit with longer storage periods, especially at the stem-end of the fruit. Nitroblue tetrazolium reducing activity, an indication of superoxide anion radical generation, was reduced by 1-MCP at both storage temperatures. H2O2 levels were inconsistently affected by 1-MCP treatment, while malondialdehyde levels, indicating lipid peroxidation, were higher in 1-MCP treated than untreated fruit at 0.5 degrees C, but inconsistently affected by 1-MCP in fruit at 3.3 degrees C. Ascorbic acid concentrations were lower in 1-MCP treated fruit at the end of storage at both temperatures but dehydroascorbic acid concentrations were lower by 1-MCP at 3.3 degrees C from week 15 to week 30. While glutathione concentrations of reduced and oxidized forms were not affected by 1-MCP at 0.5 degrees C, 1-MCP reduced the glutathione concentrations of the reduced form but increased that of the oxidized form at the end of storage at 3.3 degrees C. The activities of ascorbate peroxidase, monodehydroascorbate reductase, dehydroascorbate reductase and glutathione reductase were not affected consistently by storage temperature or 1-MCP treatment. Temperature and 1-MCP treatment effects on superoxide dismutase (SOD) activity were also inconsistent, while Cu/Zn-SOD activity was reduced in 1-MCP treated fruit stored at 3.3 degrees C. Catalase activity was not affected by 1-MCP at 3.3 degrees C, but at 0.5 degrees C its activity gradually increased in 1-MCP treated fruit before returning to lower levels by the end of storage. 1-MCP reduced the activity of peroxidase at 0.5 degrees C but increased its activity at 3.3 degrees C by the end of the storage period. Overall, the results do not indicate that a direct role of antioxidant metabolism during development of flesh browning in ‘Empire’ apples but partial least square analysis revealed that the activity of ascorbate peroxidase might be the candidate metabolite in flesh browning development at 3.3 degrees C.