Cadmium (Cd) is a non-essential trace element that elicits oxidative stress. Plants respond to Cd toxicity via increasing their Cd-chelating and antioxidative capacities. They predominantly chelate Cd via glutathione (GSH) and phytochelatins (PCs), while antioxidative defence is mainly based on the use and recycling of both GSH and ascorbate (AsA), complemented by superoxide dismutase (SOD) and catalase (CAT). In addition, both metabolites act as a substrate for the regeneration of other essential antioxidants, which neutralize and regulate reactive oxygen species (ROS). Together, these functions influence the concentration and cellular redox state of GSH and AsA.
Jozefczak et al. study the responses of mutant Arabidopsis thaliana plants deficient in glutathione (GSH) and ascorbate (AsA) when exposed to Cd toxicity and find that GSH and AsA deficiency differentially alter plant GSH homeostasis, resulting in opposite Cd sensitivities relative to wild-type plants. GSH-deficient mutants are hampered in chelation and experience phenotypic disturbances and even more oxidative stress, and therefore activate multiple alternative pathways such as SOD, CAT and APx, indicating a higher Cd sensitivity. Ascorbate deficiency, however, is associated with enhanced synthesis of phytochelatins and GSH in comparison to wild-type plants after Cd exposure, which contributes to decreased sensitivity towards Cd.
This article appears in the special issue ROS and NO Reactions in Plants.