Involvement of lipoxygenase, lipoxygenase pathway volatiles, and lipid peroxidation during the hypersensitive reaction of pepper leaves to Xanthomonas campestris pv. vesicatoria

Lipoxygenase activity and protein, production of lipid-derived volatiles, and lipid peroxidation levels were determined in pepper (Capsicum annuum L., cv. Early Calwonder-10R) leaves during the hypersensitive reaction induced by avirulent race 2 of Xanthomonas campestris pv. vesicatoria. Lipoxygenase activity increased during the collapse phase of the hypersensitive reaction (8 to 12 h after inoculation), and an increase in electrolyte leakage occurred. However, Western blot analysis revealed thai lipoxygenase proteins decreased during the same period. When only one longitudinal half of a pepper leaf was inoculated with the avirulent bacterium race, a significant increase in lipoxygenase activity was observed in both inoculated and noninoculated leaf halves, 10 h after inoculation. In addition, lipoxygenase protein decreased in inoculated leaf halves, but remained unchanged in noninoculated ones. The evolution of some volatile compounds derived from the lipoxygenase pathway [(E, E)-2,4-hexadienal, 1-hexanol, 3-hexen-1-ol, 2,4-hexadienal and 2,4-eptadienal] and carotenoid degradation (alpha- and beta-ionone) increased in the incompatible interaction during the collapse phase of the hypersensitive reaction. The level of the oxidative index (A(235)/A(205)) of leaf lipid extracts, determined to estimate lipid peroxidation, significantly increased in the advanced stage of the hypersensitive reaction. Furthermore, determination of the oxidative index in neutral lipid, glycolipid and phospholipid fractions showed that the oxidative index was significantly increased only in the glycolipid fraction. Lipoxygenase activity and protein, electrolyte leakage, volatiles and lipid peroxidation were nor changed in pepper leaves inoculated with the virulent race 1 of X. campestris pv. vesicatoria during the time interval considered (2-12 h after inoculations). The hypothesis that a lipoxygenase with chloroplastic location is induced in the incompatible interaction, and which is responsible for the increase in lipid peroxidation is advanced. (C) 1999 Academic Press.