General Effects

Sharma and Agrawal (2005) described the general effects of heavy metals on plant physiological processes. Because it can be easily measured, plant growth is commonly used as a general parameter to study the influence of stressors, with growth rate inhibition often being the most obvious plant reaction (Fodor 2002; Hagemeyer 2004). This is especially true of the root system, which is the first plant system to come into direct contact with toxic ions. Leaf chlorosis, disturbed water balance and reduced stomatal opening are characteristic effects of toxic Ni concentrations (Clemens 2006), but they are also caused by many heavy metals (as part of heavy metal toxicity syndrome) and even occur more generally as a stress response.

Fodor (2002) suggested an interesting stepwise model for the action of heavy metals in plants. Initially, there are interactions with other ionic components present at the locus of entry into the plant rhizosphere that subsequently have consequences for the metabolism. This is followed by an impact on the formation of reactive oxygen species (ROS) in the cell wall and an influence on the plasmalemma membrane system (stage 1). At stage 2, the metal ion reacts with all possible interaction partners within the cytoplasm, including proteins, other macromolecules and metabolites. Stage 3 is mainly related to the factors that influence homeostatic events, including water uptake, transport and transpiration. At this stage, symptoms start to develop, and they become visible at stage 4 according to Fodor's model. As an example, the chlorophyll and, usually to a smaller degree, carotenoid contents decrease, which have obvious consequences for photosynthesis and plant growth (Barcelo and Poschenrieder 2004). The death of the plant cell occurs at stage 5. This model has the advantage that visible effects are linked to metabolic events that are influenced by the metal ion of interest.

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