Salicylic Acid Is a Modulator of Tobacco and Mammalian Catalases

Abstract

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 H 2 O 2 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 H 2 O 2 fluxes were relatively low (1 M/min or less), SA inhibited catalase, consistent with its suggested signaling function via H 2 O 2 . However, significant inhibition was only observed at 100 M 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 H 2 O 2 (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.

Salicylic acid-induced superoxide generation catalyzed by plant peroxidase in hydrogen peroxide-independent manner

“…1A). 19,33 SA has affinity for various forms of heme proteins such as native form of catalase 8, 9 and ascorbate peroxidase, 15 Compound II of HRP 18 and SBP, 32 and Compound III of HRP. 19 We can expect that SA may interact with native form of plant peroxidases.…”

“…[1][2][3] Early studies have indicated that SA is an active signal accompanying oxidative burst by which development of systemic acquired resistance (SAR) against a wide range of pathogens is induced, as reviewed in several articles by our group. [2][3][4][5][6] In 1990s, it has been proposed that SA signaling paths leading to SAR require the accumulation of ROS derived from H 2 O 2 , 7 based on the observation that SA binds and inhibits 2 types of H 2 O 2 -detoxifying enzymes, namely catalase 8, 9 and ascorbate peroxidase. 10 In addition to these passive modes of ROS production by SA, more active modes of SA action involving extracellular peroxidase and NADPH oxidase that directly generates ROS in the presence of SA was reported later.…”

Salicylic Acid Is a Reducing Substrate and Not an Effective Inhibitor of Ascorbate Peroxidase

“…It has been reported that SA radicals derived from the catalase oxidation-reduction cycle could facilitate lipid peroxidation, which in turn activates PR-1 genes in tobacco cells (14). It is important to note that APX is a much better oxidant of SA than is catalase.…”

“…Apparently, in different plants under certain environmental conditions other products of detoxification of SA may also be formed. Further in vivo studies are necessary to define the mechanism of detoxification of SA by APX.It has been reported that SA radicals derived from the catalase oxidation-reduction cycle could facilitate lipid peroxidation, which in turn activates PR-1 genes in tobacco cells (14). It is important to note that APX is a much better oxidant of SA than is catalase.…”

“…Klessig and co-workers (12)(13)(14) have suggested that one mechanism of SA action is to inhibit catalase and ascorbate peroxidase (APX) (15), thereby elevating the endogenous levels of H 2 O 2 , that result from either the oxidative burst associated with the hypersensitive response following pathogen attack or from metabolic processes (e.g. photorespiration, photosynthesis, and oxidative phosphorylation).…”