1-MCP Regulates Ethanol Fermentation and GABA Shunt Pathway Involved in Kiwifruit Quality During Postharvest Storage

Abstract

Kiwifruit (Actinidia deliciosa) ‘Bruno’ is prone to accumulate ethanol rapidly after respiratory climacteric during storage at ambient conditions without stresses, which causes quality deterioration of the fruit associated with alcohol off-flavor. For maintaining the postharvest quality of kiwifruit ‘Bruno’, the effects of 1.0 µL • L−1 1-methylcyclopropene (1-MCP) treatment on regulating the ethanol fermentation and γ-aminobutyric acid (GABA) shunt pathway associated with control of alcohol off-flavor were investigated during storage at room temperature (24 ± 1) °C for 27 days. The results showed that 1-MCP treatment significantly reduced the respiration rate, ethylene production, decay rate, ascorbic acid (AsA) loss, and delayed the decline in the firmness and titratable acidity (TA), and the increase in total soluble solid (TSS) in kiwifruit. Furthermore, 1-MCP treatment effectively inhibited the increases in contents of acetaldehyde, ethanol, and GABA along with the suppressed activities of key enzymes involved in ethanol fermentation and GABA shunt pathway, such as pyruvate decarboxylase (PDC), alcohol dehydrogenase (ADH), glutamate decarboxylase (GAD), and GABA-transaminase (GABA-T) in kiwifruit during storage. In conclusion, 1-MCP treatment efficiently regulated the ethanol fermentation and GABA shunt pathway by delaying the ripening process to avoid the alcohol off-flavor development, thereby contributed to maintaining the quality of the kiwifruit.