Anthropogenic pollution of agricultural soils with cadmium (Cd) should receive adequate attention as Cd accumulation in crops endangers human health. When Cd is present in the soil, plants are exposed to it throughout their entire life cycle. As it is a non-essential element, no specific Cd uptake mechanisms are present. Therefore, Cd enters the plant through transporters for essential elements and consequently disturbs plant growth and development. In this review, we will focus on the effects of Cd on the most important events of a plant’s life cycle covering seed germination, the vegetative phase and the reproduction phase. Within the vegetative phase, the disturbance of the cell cycle by Cd is highlighted with special emphasis on endoreduplication, DNA damage and its relation to cell death. Furthermore, we will discuss the cell wall as an important structure in retaining Cd and the ability of plants to actively modify the cell wall to increase Cd tolerance. As Cd is known to affect concentrations of reactive oxygen species (ROS) and phytohormones, special emphasis is put on the involvement of these compounds in plant developmental processes. Lastly, possible future research areas are put forward and a general conclusion is drawn, revealing that Cd is agonizing for all stages of plant development.

The toxic metal cadmium (Cd) is a major soil pollutant. Knowledge on the acute Cd-induced stress response is required to better understand the triggers and sequence of events that precede plant acclimation. Therefore, we aimed to identify the pressure points of Cd stress using a short-term exposure set-up ranging from 0 h to 24 h. Acute responses related to glutathione (GSH), hydrogen peroxide (H₂O₂), 1-aminocyclopropane-1-carboxylic acid (ACC), ethylene and the oxidative challenge were studied at metabolite and/or transcript level in roots and leaves of Arabidopsis thaliana either exposed or not to 5 µM Cd. Cadmium rapidly induced root GSH depletion, which might serve as an alert response and modulator of H₂O₂ signalling. Concomitantly, a stimulation of root ACC levels was observed. Leaf responses were delayed and did not involve GSH depletion. After 24 h, a defined oxidative challenge became apparent, which was most pronounced in the leaves and concerted with a strong induction of leaf ACC synthesis. We suggest that root GSH depletion is required for a proper alert response rather than being a merely adverse effect. Furthermore, we propose that roots serve as command centre via a.o. root-derived ACC/ethylene to engage the leaves in a proper stress response.

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 cadmium-sensitive 2-1 (cad2-1) mutant. Cadmium-induced root and leaf responses related to oxidative challenge, hydrogen peroxide (H₂O₂), GSH, ethylene, and 1-aminocyclopropane-1-carboxylic acid (ACC) were compared between wild-type (WT) and mutant Arabidopsis thaliana plants. Although the cad2-1 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 cad2-1 mutant plants and the lack of proper transient ethylene signalling contributed to this suboptimal acclimation, resulting in a more pronounced Cd effect.