Role of dynamics of intracellular calcium in aluminium-toxicity syndrome.

This review is concentrating on the role of aluminium (Al)-calcium (Ca) interactions in Al toxicity syndrome in plants. Disruption of cytoplasmic Ca homeostasis has been suggested as a primary trigger of Al toxicity. Aluminium causes an increase in cytosolic Ca activity, potentially disrupting numerous biochemical and physiological processes, including those involved in the root growth. The source of Ca for the increase in cytosolic Ca activity under Al exposure is partly extracellular (likely to be due to the Al-resistant portion of the flux through depolarization-activated Ca channels and fluxes through Ca -permeable nonselective cation channels in the plasma membrane) as well as intracellular (increased cytosolic Ca activity enhances the activity of Ca release channels in the tonoplast and the endoplasmic reticulum membrane). The effect on increased cytosolic Ca activity of possible Al-related inhibition of the plasma membrane and endo-membrane Ca -ATPases and Ca exchangers (CaX) that sequester Ca out of the cytosol is insufficiently documented at present. The relationship between Al toxicity, cytoplasmic Ca homeostasis and cytoplasmic pH needs to be elucidated. Technical improvements that would allow measurements of cytosolic Ca activity within the short time after exposure to Al (seconds or shorter) are eagerly awaited. Contents I. Introduction 296 II. Symptoms of aluminium toxicity 296 III. Calcium - aluminium interactions 297 IV. The role of electrical properties of the plasma membrane in calcium-aluminium interactions 306 V. Oxidative stress 307 VI. Callose 308 VII. Cytoskeleton 308 VIII. Conclusions 309 Acknowledgements 309 References 309.