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.