Exogenous γ-Aminobutyric Acid Delays Chilling Injury of Harvested Kiwifruit and Relates with Reactive Oxygen Species Metabolism

Abstract

The effect of γ-aminobutyric acid (GABA) treatment on chilling injury in cold-stored kiwifruit and its relationship with reactive oxygen species (ROS) metabolism were investigated. Postharvest kiwifruit were treated with 2.0 mmol/L GABA solution for 20 min and stored at (4 ± 1) ℃ and (85 ± 5)% relative humidity. Chilling injury development was evaluated and the changes in the dynamic balance between the production and removal of ROS were analyzed. The results showed that compared with the control group, GABA treatment could delay the increases in the chilling injury index, cell membrane permeability and malondialdehyde (MDA) content of cold-stored kiwifruit, inhibit the rate of superoxide anion radical production and the increase in hydrogen peroxide content, and increase and maintain superoxide dismutase (SOD), catalase (CAT), ascorbate peroxidase (APX), glutathione reductase (GR), monodehydroascorbate reductase (MDHAR) and dehydroascorbate reductase (DHAR) activities. Moreover, GABA treatment slowed down the decrease in the contents of ascorbic acid and glutathione, which contributed to higher antioxidant capacity levels in the fruit. The above findings indicated that exogenous GABA treatment could maintain dynamic redox balance, attenuate membrane lipid peroxidation and preserve cell membrane integrity in cold-stored kiwifruit by inhibiting the accumulation of ROS, and increasing the activities of the enzymatic and non-enzymatic ROS systems, thereby enhancing cold stress resistance and ultimately delaying chilling injury.

Keywords

• kiwifruit; γ-aminobutyric acid; chilling injury; reactive oxygen species; ascorbate-glutathione cycle