Mechanisms of Aluminum Toxicity in Plants

Controversy exists over mechanisms of aluminum phytotoxic effects (96-99). Researchers long have debated whether the primary toxic effect of aluminum is on inhibition of cell elongation or inhibition of cell division. Lazof and Holland (28) demonstrated in soybean, pea (Pisum sativum L.), and bean (Phaseolus vulgaris L.) that both effects occur, with rapid, largely reversible responses to aluminum toxicity due to cell extension effects and irreversible responses due to cell division effects.

Another question puzzling researchers is whether the primary injury due to aluminum in plants is symplasmic or apoplastic. Horst (100) and Horst et al. (101) reviewed the evidence supporting the apoplast as the site of the primary aluminum-toxic event. However, dividing aluminum effects into symplasmic or apoplastic can be arbitrary, because aluminum could enter the symplasm to produce effects in the cell wall or outer face of the plasma membrane.

Since cell walls occur in plants and not animals, aluminum injuries at this site are unique to plants. Possible mechanisms of aluminum injury in cell walls include: (a) aluminum binding to pectin; or (b) modification of synthesis or deposition of polysaccharides. Jones and Kochian (102) proposed that the plasma membrane is the most likely site of aluminum toxicity in plants. Possible mechanisms of toxicity in the plasma membrane are: (a) aluminum binding to phospholipids; (b) interference with proteins involved in transport; or (c) signal transduction. Once aluminum enters the symplasm, there are many possible interactions with molecules containing oxygen donor ligands (47,48). Probable mechanisms of aluminum toxicity within plant cells include: (a) disruption of the cytoskeleton, (b) disturbance of calcium homeostasis, (c) interaction with phytohormones, (d) oxidative stress, (e) binding to internal membranes in chloroplasts, or (f) binding to nuclei.