Growth of the plant was optimal at 10 nM Cu, while PSII activity (Fv/Fm) was maximal around 2 nM Cu. The main storage site for Cu up to physiological concentrations was in the vein.
At toxic copper concentrations, damage to the PSII reaction centre was the first target of inhibition, followed by disturbed regulation of heat dissipation (NPQ). Only after that, electron transport through PSII (ΦPSII) was inhibited, and finally chlorophylls decreased. Copper accumulation in the plants was stable until 10 nM Cu in solution, but strongly increased at higher concentrations. At toxic levels Cu was sequestered from the vein to the epidermis and mesophyll, until export from the vein became inhibited. This re-distribution of Cu was accompanied by inhibition of Zn uptake.
Copper deficiency leading to a complete stop of growth was accompanied by high starch accumulation, although electron flow through PSII (ΦPSII) decreased from 2 weeks. This was followed by a decrease in pigments and increase of non photochemical quenching (NPQ). Release of Cu from the plants below 10 nM Cu supply in the nutrient solution indicated lack of high-affinity Cu transporters. On the tissue level, copper deficiency led to a re-distribution of zinc.