Cadmium (Cd) is a non-essential metal that elicits oxidative stress. Plants respond to this Cd toxicity via increasing their chelating and antioxidative capacities. They predominantly chelate Cd via glutathione (GSH) and phytochelatins (PCs), while antioxidative responses are 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 cellular redox state of GSH and AsA, which includes both their concentration and reduction/oxidation ratio. In this study, both parameters concerning GSH and AsA redox state were taken into consideration in plants exposed to sublethal Cd concentrations. Deficiency in GSH (cad2-1 mutant), AsA (vtc1-1 mutant) and both metabolites (cad2-1 vtc1-1 mutant) demonstrated changes in plant GSH homeostasis under control conditions, resulting in different Cd sensitivities. In comparison to wild-type plants, elevated basal thiol levels and enhanced PC synthesis upon Cd exposure efficiently compensated AsA deficiency in vtc1-1 plants and contributed to decreased sensitivity towards Cd. Glutathione deficient (cad2-1 and cad2-1 vtc1-1) mutants however, showed a more oxidized GSH redox state, resulting in initial oxidative stress and a higher sensitivity to Cd. In order to cope with the present Cd stress, GSH deficient mutants activated multiple alternative pathways.