Role of dynamics of intracellular calcium in aluminium-toxicity syndrome

Abstract

This review is concentrating on the role of aluminium (Al)-calcium (Ca) interactions in Al toxicity syndrome in plants. Disruption of cytoplasmic Ca²⁺ homeostasis has been suggested as a primary trigger of Al toxicity. Aluminium causes an increase in cytosolic Ca²⁺ activity, potentially disrupting numerous biochemical and physiological processes, including those involved in the root growth. The source of Ca²⁺ for the increase in cytosolic Ca²⁺ activity under Al exposure is partly extracellular (likely to be due to the Al-resistant portion of the flux through depolarization-activated Ca²⁺ channels and fluxes through Ca²⁺ -permeable nonselective cation channels in the plasma membrane) as well as intracellular (increased cytosolic Ca²⁺ activity enhances the activity of Ca²⁺ release channels in the tonoplast and the endoplasmic reticulum membrane). The effect on increased cytosolic Ca²⁺ activity of possible Al-related inhibition of the plasma membrane and endo-membrane Ca²⁺ -ATPases and Ca²⁺ exchangers (CaX) that sequester Ca²⁺ out of the cytosol is insufficiently documented at present. The relationship between Al toxicity, cytoplasmic Ca²⁺ homeostasis and cytoplasmic pH needs to be elucidated. Technical improvements that would allow measurements of cytosolic Ca²⁺ 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.

Keywords: H+-ATPase; aluminium (Al); calcium (Ca); callose; cytoplasmic Ca2+ homeostasis; cytoskeleton; plasma membrane; secondary messenger system.