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
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.