| Summary: | Pollution by cadmium (Cd) is a worldwide problem, posing risks to human health and impacting crop yield and quality. Cadmium-induced phytotoxicity arises from an imbalance between antioxidants and pro-oxidants in favour of the latter. The Cd-induced depletion of the major antioxidant glutathione (GSH) strongly contributes to this imbalance. Rather than being merely an adverse effect of Cd exposure, the rapid depletion of root GSH levels was proposed to serve as an alert response. This alarm phase is crucial for an optimal stress response, which defines acclimation later on. To obtain a better understanding on the importance of GSH in the course of these responses and how these are defined by the rapid GSH depletion, analyses were performed in the GSH-deficient <i>cadmium-sensitive 2-1</i> (<i>cad2-1</i>) mutant. Cadmium-induced root and leaf responses related to oxidative challenge, hydrogen peroxide (H<sub>2</sub>O<sub>2</sub>), GSH, ethylene, and 1-aminocyclopropane-1-carboxylic acid (ACC) were compared between wild-type (WT) and mutant <i>Arabidopsis thaliana</i> plants. Although the <i>cad2-1</i> mutant has significantly lower GSH levels, root GSH depletion still occurred, suggesting that the chelating capacity of GSH is prioritised over its antioxidative function. We demonstrated that responses related to GSH metabolism and ACC production were accelerated in mutant roots and that stress persisted due to suboptimal acclimation. In general, the redox imbalance in <i>cad2-1</i> mutant plants and the lack of proper transient ethylene signalling contributed to this suboptimal acclimation, resulting in a more pronounced Cd effect.
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