ABSTRACT
ROS are part of plant metabolism and their major sources are (1) oxygen reduction by organellar electron transport (in chloroplasts or mitochondria) yielding superoxide anion radicals (O2-•), (2) peroxisomes that produce hydrogen peroxide (H2O2) by the enzymatic activity of glycolate oxidase, and (3) plasma membrane NADPH-dependent oxidases generating O2-•. These ROS are linked by the O2-• → H2O2 → H2O series of reactions that may occur either spontaneously (O2-• → H2O2) or catalyzed by enzymes (O2-• → H2O2, by superoxide dismutases; H2O2 → H2O, by peroxidases). Metal ions, such as Fe2+ or Cu+, catalyze the H2O2 → •OH reaction, yielding a strongly oxidizing hydroxyl radical (Apel and Hirt, 2004; Møller, 2001). In chlorophyll-containing cells an additional source is a pigment-photosensitized production of singlet oxygen (1O2) (Triantaphylidès et al., 2008). With the exception of H2O2, all ROS have short, submillisecond lifetimes in leaves. Under standard metabolic conditions, ROS concentrations are strictly controlled and kept low by antioxidants in all plant tissue. Stress conditions, however, upset this balance of ROS production and neutralize it either by weakening the antioxidant system or increasing the production of pro-oxidants. Increased leaf ROS concentrations are reportedly associated with a variety of abiotic and biotic stresses (Bailey-Serres and Mittler, 2006). Excess ROS causes biological damage either directly, at their production site by oxidizing cellular components, or indirectly, by generating other oxidants capable of traveling inside cells or even passing through membranes. Such latter reactions support the idea of certain ROS or their derivatives acting as signal molecules and being part of defensive cellular responses rather than acting as damaging agents (Mittler et al., 2004; Pitzschke et al., 2006; Fischer et al., 2013).
