Abstract

Linoleate oxidation by avocado lipoxygenase was inhibited in vitro in the presence of the specific inhibitor 5,8,11,14-eicosatetraynoic acid (ETYA). Infiltration with ETYA of avocado discs inoculated with Colletotrichum gloeosporioides delayed symptom development at concentrations where the fungus itself was not affected. Subsequently, a natural inhibitor of avocado lipoxygenase was isolated from peels of unripe avocado fruits and identified as epicatechin. It inhibited avocado lipoxygenase with a K i of 0·64 μm. The concentration of epicatechin in unripe fruits was 514 μg g − fresh weight of peel; this decreased during ripening to 8 μg g −1 fresh weight, before symptoms of C. gloeosporioides infections were expressed. A comparison of two cultivars with differing susceptibility to C. gloeosporioides showed that the concentration of epicatechin decreased faster in the cultivar in which symptoms appeared first. An atmosphere containing 50 μg l − ethylene enhanced the decrease of the lipoyxygenase inhibitor in avocado fruits and shortened the period before symptoms of disease were expressed. In over-mature, firm and naturally infected fruits hanging in the orchard the concentration of epicatechin was 260 μg g − in the area of the peel without symptoms and only 27 μg g − in that showing symptoms of infection. The results are discussed in relation to the hypothesis that the latency of the infection of avocado fruit by C. gloeosporioides may be accounted for by the degradation of the preformed antifungal compound, cis,cis-1-acetoxy-2-hydroxy-4-oxo-heneicosa-12, 15-diene, which is catalysed by avocado lipoxygenase, and that the in vivo lipoxygenase activity may increase during ripening owing to the decline in the levels of its endogenous inhibitor epicatechin.

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