This review spotlights on recent indications that recognizes potential cellular mechanisms that may be involved in the tolerance of salicylic acid (SA)-treated seedlings to the presence of cadmium (Cd) in their environment. It appears probable that SA stimulates signaling systems implicated in plant defense-related actions against Cd-induced oxidative stress. These include mechanisms that reduce uptake of metals into the cytosol by extracellular chelation through extruded ligands and binding onto cell-wall constituents. Cellular chelation of metals in the cytosol by a range of ligands (peptides, phytochelatins (PCs)), or increased efflux from the cytosol out of the cell or into sequestering compartments are also key mechanisms improving tolerance. Free-radical scavenging capacities through the activity of antioxidant enzymes or production of peptides and PCs add another line of defense against the toxic effect of Cd. The SA signaling events can be attributed to the extracellular SA perception model in which reactions between SA and apoplastic proteins result in acute oxidative burst under Cd stress.
