i " i ■ 100(im 000422.

FIGURE 20.2 Scanning electron micrographs of untreated tomato (A1), pepper calyx (B1), and melon (C1) compared to HWRB-treated tomato (A2), pepper calyx (B2), and melon (C2) (s, fungal spores; h, hyphae; dp, dirt particles).

in the defense systems against pathogens that slowed fungal development as a result of heat-induced changes in the fruit tissue. Heat treatments induced the biosynthesis of lignin-like polymers that were bound to walls of cells adjacent to wound sites in citrus peel [64]. HWRB treatment of 52°C for 15 seconds induced tomato resistance when fruit was artificially inoculated with B. cinerea 24 hours after treatment [90]. HWRB treatment at 62° C for 20 seconds was most effective in inducing disease resistance against green mold (P. digitatum) when grapefruit was inoculated after 1 and 3 days after treatment [91]. The HWRB treatment induced the accumulation of proteins that cross-reacted with heat shock proteins and of proteins that cross-reacted with chitinase and 1,3-glucanase antibodies [61]. The increases in the accumulation of chitinase and glucanase proteins, which were detected 1 and 3 days after

HWRB treatment, may be part of the complex fruit resistance mechanisms induced by this technology [31,91]. The mode of action of the hot water dip in reducing the decay of lemon fruit is partly related to the temporary thermal inhibition of pathogen growth that allowed the infected fruit to build up production of lignin-like material at the inoculation site, followed later by accumulation of the phytoalexins scoparone and scopolitin [63].

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