Role of dynamics of intracellular calcium in aluminium-toxicity syndrome

Authors

  • Z. Rengel,

    Corresponding author
    1. Soil Science and Plant Nutrition, School of Earth and Geographical Sciences, The University of Western Australia, 35 Stirling Highway, Crawley WA 6009, Australia;
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  • W.-H. Zhang

    1. Department of Horticulture, Viticulture & Oenology, Waite Campus, Adelaide University, PMB #1, Glen Osmond SA 5064, Australia
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Author for correspondence: Z. Rengel Fax: +618 93801050 Email: zrengel@agric.uwa.edu.au

Abstract

Contents

  • I. Introduction  000
  • II. Symptoms of aluminium toxicity  000
  • III. Calcium – aluminium interactions  000
  • IV. The role of electrical properties of the plasma membrane in calcium–aluminium interactions  000
  • V. Oxidative stress  000
  • VI. Callose  000
  • VII. Cytoskeleton  000
  • VIII. Conclusions  000
  • Acknowledgements  000

  • References  000

Summary

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.

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