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


  • 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


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.