Wounding plant tissues elicits the production of a wound signal which propagates into adjacent tissue and initiates a number of genetically programmed responses. Over their evolutionary history, plants have acquired a limited number of responses to adverse conditions. Each type of stress does not therefore evoke a unique response, but different types of stresses (e.g. mechanical damage from cutting, insect feeding, or flexing in the wind; exposure to toxic levels of certain chemicals; exposure to phyto-active levels of plant growth regulators like ethylene) often elicit similar responses. While adaptive in their original setting, many of these reactions produce unwanted affects in harvested tissue.

Many stresses induce increased phenylpropanoid metabolism with the synthesis and accumulation of phenolic compounds. Simple phenolic compounds (e.g. cinnamic acid, chlorogenic acid) can directly discourage insect feeding, or provide the substrates for further synthesizing and polymerizing reactions that produce lignin to strengthen cell walls and isolate injured or diseased areas of the plant. Toughening of harvested asparagus is a good example of how harvest-induced injuries promote phenolic synthesis, and the subsequent lignification and toughening of the supportive stem tissue. While the stress-induced increase in the production of phenolic compounds is beneficial for the survival of the plant in the field, it is often objectionable in harvested fresh fruits and vegetables.

The level of phenolic compounds varies greatly among fruits and vegetables, within their various tissues and over time. Young fruit have higher levels of phenolic compounds than ripe fruit, while younger vegetative tissue has lower levels than more mature tissue. Artichokes, apples and potatoes, for example, have relatively high levels of phenolic compounds constitutively, and rapidly brown when cut. In contrast, lettuce has low levels of phenolic compounds and the synthesis and accumulation of wound-induced phenolic compounds significantly increase the development of tissue browning. Development of strategies to control tissue browning must therefore be tailored to the requirements of the specific commodity and form in which it is marketed (e.g. whole or fresh-cut). Antioxidants can lessen the browning of phenolic compounds already present in the tissue, while interfering with phenolic synthesis can prevent the accumulation of sufficient concentrations to produce browning in tissue with low levels of indigenous phenolic compounds.

Wounding also promotes increased respiration, ethylene production, water loss and senescence. By disrupting the protective epidermal and cuticular layers it also offers an entry point for pathogens. The expansion of the market for fresh-cut fruits and vegetables has increased the need for a better understanding of the processes elicited by wounding and how they can be controlled.

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