Wounding and ultraviolet radiation stresses affect the phenolic profile and antioxidant capacity of carrot tissue

Abiotic stresses have been known to induce the production of secondary metabolites in plants as part of the defense mechanism systems. Many of these compounds were reported to have bioactive properties, such as antioxidant, antimutagenic, antimicrobial, or anticarcinogenic. By using these stresses as tools, it is possible to develop strategies to produce fruits and vegetables with higher health promoting compounds. We determined that wounding and UV radiation caused total phenolics, antioxidant capacity (AOX), and PAL enzyme activity to increase significantly. This increase is affected by wounding intensity, time period of UV exposure, and duration of storage. There was no significant difference between the cultivars tested (Navajo, Legend, and Choctaw). The main phenolic compounds identified for all cultivars using HPLC-DAD were chlorogenic acid and its isomers (dicaffeoylquinic acids), ferulic acid, phydroxybenzoic acid and its derivative, p-coumaric acid derivative, and isocoumarin. Combining wounding with different UV lights (A, B, and C) induced the production of different phenolic compounds. The type of phenolics induced depended on the type of UV radiation used. The synthesized phenolic compounds showed a high linear relationship with AOX capacity. The specific antioxidant activity induced by each stress treatment depended on the induced phenolic profile. Reactive oxygen species (ROS), jasmonic acid (JA), and ethylene are all involved as secondary signaling molecules in the wounding and UV stress-induced phenolic metabolism. This is shown by the decrease in the synthesis of total phenolic compounds in stressed carrot tissue when using diphenyleneiodonium chloride (DPI), phenidone, or 1-methylcyclopropene (1-MCP), which inhibit NADPH oxidase (ROS production), lipoxygenase (key enzyme in JA metabolic pathway), and block ethylene receptor, respectively. These inhibitors showed a dose response effect by reducing the synthesized phenolic compounds. This information, plus the combined effects of the inhibitors enabled us to propose a possible signaling mechanism of stress-induced phenolic synthesis caused by wounding and different UV radiations. Abiotic stresses, such as wounding and UV radiation, elicit the synthesis of phenolic compounds, increasing the antioxidant capacity of the tissue. This approach shows the potential of using plant stress-induced signaling mechanisms as tools to manipulate the synthesis of desirable phenolic compounds or other secondary metabolites