Biochemical characterization of oxidative burst during interaction between Solanum lycopersicum and Fusarium oxysporum f. sp. lycopersici

The oxidative burst or rapid and transient production of large amount of reactive oxygen species (ROS) belongs to the fastest and earliest active defense responses to microbial infection known in plants. The aim of this study was to investigate the intensity and timing of the ROS formation, lipid peroxidation and expression of antioxidant enzymes as initial responses of tomato (Solanum lycopersicum L.) against the invading necrotrophic pathogen Fusarium oxysporum f. sp. lycopersici. The concentration of hydrogen peroxide (H2O2) was 2.6 times higher at 24 h post-inoculation (hpi) and lipid peroxidation was 4.4 times higher at 72 hpi in the extracts of inoculated roots than in the control. An increase in total phenolic content was also detected in inoculated roots. The activities of the antioxidative enzymes, viz., superoxide dismutase (SOD, EC 1.15.1.1), catalase (CAT, EC 1.11.1.6), guaiacol peroxidase (GPX, EC 1.11.1.7) and ascorbate peroxidase (APX, EC 1.11.1.11), increased in response to pathogen inoculation. SOD activity at 48 hpi in inoculated roots was 2.9 times that in the control. CAT activity showed a decrease after 24 hpi and the increase in activities of GPX and APX was insignificant after 24 hpi in the inoculated roots. The oxidative burst generated in the interaction between tomato and F. oxysporum f. sp. lycopersici may be an early first line of defense by the host mounted against the invading necrotrophic pathogen. However, seemingly less efficient antioxidative system (particularly the decrease of CAT activity after 24 hpi) leading to sustained accumulation of ROS and the observed higher rate of lipid peroxidation indicate that the biochemical events are largely in favour of the pathogen, thus making this host–pathogen interaction a compatible combination. It is discussed that the oxidative burst served as a weapon for the necrotrophic pathogen because the antioxidative system was not strong enough to impede the pathogen ingress in the host.