As described above, SA is involved in several abiotic stress responses in plants. Most abiotic stresses increase the in planta concentration of SA. The effect of exogenous SA application is not
obvious, but it may depend on the concentration of applied SA, mode of application, and state (developmental stage, oxidative balance, and acclimation) of the plants. Generally, low concentrations of SA application alleviate susceptibility to abiotic stresses and high concentrations of SA cause high levels of oxidative stress, leading to decreased abiotic stress tolerance (Fig. 13.2). Similarly, H2O2, which is stable, relatively long-lived, and highly permeable across membranes, acts as a signal molecule involved in acclamatory signaling at low concentrations, triggering tolerance to various abiotic and biotic stresses, but at high concentrations, it leads to programmed cell death (Quan et al. 2008). The conversion of benzoic acid into SA is catalyzed by the H2O2-mediated activation of BA2H (Dempsey and Klessig 1995). SA pretreatment also results in the accumulation of H2O2 (Agarwal et al. 2005; Harfouche et al. 2008) , Thus, it is proposed that SA and H2O2 form a self-amplifying feedback loop in response to abiotic and biotic stresses (Fig. 13.2); H2O2 induces SA accumulation, and SA enhances H2O2 level (van Camp et al. 1998).
Redox homeostasis in plant cells is maintained by the appropriate balance between ROS generation and scavenging mechanisms (Apel and Hirt 2004) . Biotic and abiotic stress conditions produce an increase in ROS levels, leading to an alteration in the cellular redox homeostasis. A number of studies demonstrate that the efficiency of antioxidative systems is correlated with tolerance to abiotic stresses (Athar et al. 2008; Munns and Tester 2008) . Application of SA at low concentrations enhances accumulation of H2O2, which induces antioxidant defense systems, including enzymatic antioxidants such as SOD (superoxide dismutase), CAT (catalase), APX (ascorbate peroxidase), and GPX (glutathione peroxidase) and nonenzymatic antioxidants such as glutathione, ascorbic acid, carotenoids, and tocopherols (Ahmad et al. 2010; Gill and Tuteja 2010). Several reports demonstrate that SA also stimulates the activity of SOD, GPX, glutathione reductase, and peroxidase (Janda et al. 1999; Milla et al. 2003; Azevedo et al. 2004; Noreen et al. 2009). The activation of ROS scavenging systems may contribute to the equilibration of ROS homeostasis to enhance abiotic stress tolerance.
High levels of SA treatment cause not only production of ROS (Kawano 2003), but also reductions in APX and CAT activity, leading to an over-accumulation of ROS (Durner and Klessig 1996; Janda et al. 2003). SA is capable of binding directly to catalase enzyme, inhibiting its activity in tobacco, Arabidopsis, tomato, maize, and cucumber (Chen et al. 1993; Sánchez-Casas and Klessig 1994; Conrath et al. 1995; Horváth et al. 2002). Over-accumulation of ROS causes oxidative damage (Ahmad et al. 2010; Gill and Tuteja 2010) and triggers both apoptosis-like and autophagic cell death (Love et al. 2008). Mitochondrial AOX (alternative oxidase) can significantly reduce electron build-up, which leads to the reduction of redox stress and ROS accumulation (Millenaar et al. 1998). Downregulation of AOX stimulates programmed cell death (Maxewll et al. 2002). Both H2O2 and SA were found to disrupt normal mitochondrial function, resulting in decreased rates of electron transport and lowering of cellular ATP levels (Norman et al. 2004). These findings suggest that the mitochondrion may play an important role in conveying intracellular stress signals to the nucleus, leading to alterations in gene expression.
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