Salicylic acid is a modulator of tobacco and mammalian catalases

Salicylic acid (SA) plays a key role in the establishment of resistance to microbial pathogens in many plants. The discovery that SA inhibits catalase from tobacco led us to suggest that H₂O₂ acts as second messenger to activate plant defenses. Detailed analyses of SA's interaction with tobacco and mammalian catalases indicate that SA acts as an electron donor for the peroxidative cycle of catalase. When H₂O₂ fluxes were relatively low (1 μM/min or less), SA inhibited catalase, consistent with its suggested signaling function via H₂O₂. However, significant inhibition was only observed at 100 μM SA or more, a level reached in infected, but not in uninfected, leaves. This inhibition was probably due to siphoning catalase into the slow peroxidative reaction. Surprisingly, SA was also able to protect catalase from inactivation by damaging levels of H₂O₂ (lower millimolar range), which is generally assumed to reflect accumulation of inactive ferro-oxy intermediates. SA did so by supporting or substituting for the protective function of catalase-bound NADPH. These results add new features to SA's interaction with heme enzymes and its in vivo redox properties. Thus, SA, in addition to its proposed signaling function, may also have an important antioxidant role in containing oxidative processes associated with plant defense responses.