Aluminium is the most important growth-limiting factor in many acid soils throughout the world. Physiological effects of Al toxicity and mechanisms of tolerance are not well understood. An initial uptake of Al is confined to the apoplasm. Aluminium complexes (whose exact identification is beyond current experimental techniques) enter the cytosol slowly and only after prolonged exposure. Electrochemical properties of the cell wall Donnan free space as well as the plasma membrane of root cells are altered by the presence of Al ions that are polyvalent cations in acidic environments. The primary Al effects are very fast (taking only seconds to several minutes to develop) and may therefore occur while Al is still in the Donnan free space and on the apoplasmic side of the plasma membrane. Resumption of root growth upon removal of Al ions supports such a claim. Aluminium affects membrane permeability for both electrolytes and non-electrolytes; it reduces accumulation of divalent cations (especially Ca and Mg) by interfering with the membrane transport. Aluminium alters the pattern of Ca2+ fluxes across the plasma membrane, thus supposedly disturbing symplasmic Ca2+ homeostasis. Supplemental Ca2+ can greatly alleviate deleterious Al effects. Frequently observed changes in the secretory activity of root cells exposed to Al are mediated through altered cell Ca2+ homeostasis; they result in cessation of cell wall growth and stoppage of root elongation. Involvement of calmodulin in the Al-related phenomena is suggested to be indirect, at least in the initial stages of the Al treatment when Al is likely to be confined to the apoplasm. The role of growth substances, at least auxins and cytokinins, in the Al toxicity syndrome appears to be related to the Ca-Al interactions that may alter the pattern of auxin transport as well as cytokinin biosynthesis and transport. Disturbance of the cell Ca2+ homeostasis appears to be an important feature of ion-related environmental stresses in general (salt, heavy metals, aluminium).