Calcium/aluminium interactions in the cell wall and plasma membrane of Chara

Abstract

The proposal that aluminium (Al) toxicity in plants is caused by either inhibition of Ca²⁺ influx or by displacement of Ca²⁺ from the cell wall, was examined. For this study the giant alga Chara corallina Klein ex Will. em. R.D. Wood was selected because it shows a similar sensitivity to Al as in roots of higher plants and, more importantly, it is possible to use the large single internodal cells to make accurate and unambiguous measurements of Ca²⁺ influx and Ca²⁺ binding in cell walls. Growth of Chara was inhibited by Al at concentrations comparable to those required to inhibit growth of roots, and with a similar speed of onset and pH dependence. At Al concentrations which inhibited growth, influx of calcium (Ca²⁺) was only slightly sensitive to Al. The maximum inhibition of Ca²⁺ influx at 0.1 mol·m⁻³ Al at pH 4.4 was less than 50%. At the same concentration, lanthanum (La³⁺) inhibited influx of Ca²⁺ by 90% but inhibition of growth was similar for both La³⁺ and Al. Removal of Ca²⁺ from the external solution did not inhibit growth for more than 8 h whereas inhibition of growth by Al was apparent after only 2.5 h. Ca²⁺ influx was more sensitive to Al when stimulated by addition of high concentrations of potassium (K⁺) or by action potentials generated by electrical stimulation. Other membrane-related activities such as sodium influx, rubidium influx and membrane potential difference and conductance, were not strongly affected by Al even at high concentrations. In isolated cell walls equilibrated in 0.5 mol·m⁻³ Ca²⁺ at pH 4.4, 0.1 mol·m⁻³ Al displaced more than 80% of the bound Ca²⁺ with a half-time of 25 min. From the poor correlation between inhibition of growth and reduction in Ca²⁺ influx, it was concluded that Al toxicity was not caused by limitation of the Ca²⁺ supply. Short-term changes in other membrane-related activities induced by Al also appeared to be too small to explain the toxicity. However the strong displacement, and probable replacement, of cell wall ca²⁺ by Al may be sufficient to disrupt normal cell development.