Mature red lychee fruit were stored at 3 different temperature and relative humidity regimes. Total anthocyanin concentration, pigment distribution, pH of the pericarp homogenate, Hunter a values (redness index), and visual colour were measured as a function of pericarp weight loss. Pericarp colour rapidly deteriorated during both ambient and high temperature storage, resulting in a uniform browning of the pericarp surface. The degree of tissue browning was proportional to the rate of pericarp desiccation. Although anthocyanin degradation occurred concurrently with tissue browning, visual colour and Hunter a values were not consistent with total anthocyanin concentration. Instead, a more significant correlation was seen between Hunter a values and the pH of the pericarp homogenate. Pericarp colour could be altered by external pH. Acidification of whole fruit increased pericarp redness, whereas alkaline treatment caused discoloration. Both colour responses occurred independently of anthocyanin synthesis and degradation and were completely reversible. These results question the current theory that browning is due to anthocyanin degradation. No evidence of browning was observed in the anthocyanin-containing mesocarp, and acidification of already brown tissue significantly increased pericarp redness independently of anthocyanin synthesis. We believe that anthocyanin pigments were progressively decolorised during ambient storage, possibly due to changes in pericarp pH. Once colourless, independent tissue browning became visual and was enhanced.

Cellular localisation of visual browning and oxidative activity studies were conducted to determine the relative significance of polyphenol oxidase (PPO) and peroxidase (POD) activities during pericarp browning. Pericarp browning was first observed on the protuberance apices and subsequently extended uniformly over the entire pericarp surface. Anatomically, browning was highly localised and restricted to the epicarp and the upper mesocarp. PPO and POD activities were highest in the epicarp, with progressively less activity in both the mesocarp and endocarp. In situ localisation of oxidative activity using tissue blots confirmed high epicarp PPO activity. POD activity, although primarily restricted to mesocarp vascular tissue, was also detected in the epicarp. We believe that litchi pericarp browning is due to highly localised oxidative activity in the epicarp and upper mesocarp. As PPO and POD activities were significantly higher in this tissue and browning was not observed when both enzymes were selectively inhibited, it is postulated that both PPO and POD activities are associated with litchi pericarp browning. The current theory that litchi pericarp browning is only caused by PPO activity needs to be re-appraised to determine the relative role of POD activity.