Aluminum Induces a Decrease in Cytosolic Calcium Concentration in BY-2 Tobacco Cell Cultures

Al toxicity is a major problem that limits crop productivity on acid soils. It has been suggested that Al toxicity is linked to changes in cellular Ca homeostasis and the blockage of plasma membrane Ca(2+)-permeable channels. BY-2 suspension-cultured cells of tobacco (Nicotiana tabacum L.) exhibit rapid cell expansion that is sensitive to Al. Therefore, the effect of Al on changes in cytoplasmic free Ca concentration ([Ca(2+)](cyt)) was followed in BY-2 cells to assess whether Al perturbed cellular Ca homeostasis. Al exposure resulted in a prolonged reduction in [Ca(2+)](cyt) and inhibition of growth that was similar to the effect of the Ca(2+) channel blocker La(3+) and the Ca(2+) chelator ethyleneglycol-bis(β-aminoethyl ether)-N,N′-tetraacetic acid. The Ca(2+) channel blockers verapamil and nifedipine did not induce a decrease in [Ca(2+)](cyt) in these cells and also failed to inhibit growth. Al and La(3+), but not verapamil or nifedipine, reduced the rate of Mn(2+) quenching of Indo-1 fluorescence, which is consistent with the blockage of Ca(2+)- and Mn(2+)-permeable channels. These results suggest that Al may act to block Ca(2+) channels at the plasma membrane of plant cells and this action may play a crucial role in the phytotoxic activity of the Al ion.