Disturbance of cell Ca²⁺ homeostasis as a primary trigger of Al toxicity syndrome

The primary toxic effects of Al are fast (taking only seconds to several minutes to develop). These effects may be due to the presence of Al ions on the apoplasmic side of the plasma membrane; Al ions may not need to enter the cytosol for a range of primary deleterious Al effects to occur. Aluminium may disturb the symplasmic Ca²⁺ homeostasis by altering the pattern of Ca²⁺ fluxes across the plasma membrane. Disturbance of transmembrane Ca²⁺ fluxes may prevent an increase in cytosolic Ca²⁺ activity necessary to trigger spindle formation during prophase as well as to initiate the metaphase/anaphase transition. The mechanism behind Al‐related inhibition of mitosis and polar cell growth is suggested to be disturbance of stimulus/response coupling effected through Ca²⁺ as a second messenger. Involvement of calmodulin in the Al‐related phenomena could be indirect, at least in the initial stages of the Al treatment when Al is probably confined to the apoplasm only. Al‐related disturbance of the Ca²⁺ homeostasis in the cytosol would alter the patterns of Ca²⁺ ‐calmodulin binding, resulting in the absence of activation or only partial activation of calmodulin.