The role and mode of action of UV-C hormesis in reducing cellular oxidative stress and the consequential chilling injury of banana fruit peel

The reduction of cellular oxidative stress causing chilling injury (CI) of banana fruit peel by UV-C hormesis was investigated. Banana [Musa (AAA group, Cavendish subgroup) cv. Cavendish] fruits were treated with UV-C at dosages of 0.02 kJ m^-², 0.03 kJ m^-² or 0.04 kJ m^-² prior to storage at 5 and 25°C. Symptoms of CI were observed when fruits stored at 5°C and severity was increased with time of storage. However, UV-C treatment reduced both the incidence of CI and its severity compared with controls. UV-C treatment activated phenylalanine ammonia-lyase and resulted in higher levels of total phenolic compounds in comparison with untreated controls. Our results showed that oxidative stress caused by CI in banana resulted from the accumulation of reactive oxygen species (ROS) intermediates such as H2O2 and superoxide anion, and at CI-inducing temperatures, a marked increased in H2O2 content was observed. However, UV-C treatment led to significantly higher activities of superoxide dismutase, catalase, peroxidase, ascorbate peroxidase, and glutathione reductase compared to control fruit during later storage. The activation of antioxidants by UV-C treatment reduced cellular oxidative stress damage, as indicated by lower levels of malondialdehyde and DNA degradation. In addition, heat-shock protein (HSP) 70 gene expression was increased by UV-C treatment, suggesting a possible mode of action of UV-C in the prevention of cellular damage and maintenance of cellular homeostasis. Taken together, these results suggest that the development of CI symptoms in banana fruit are associated with ROS accumulation, and UV-C treatment, by activation of defense mechanisms such as antioxidant enzymes and HSP70 gene expression, can reduce cellular oxidative stress, thus preventing membrane degradation and DNA damage associated with CI.