One explanation for AI toxicity in plants suggests that AI displaces ca'+ from critical sites in the apoplasm. We evaluated the Ca'+-displacement hypothesis directly using near-isogenic lines of wheat (Triticum aestivum L.) that differ in AI tolerance at a single locus. We measured both the growth and total accumulation (apoplasmic plus symplasmic) of 45Ca and AI into roots that had been exposed to AI alone or to AI with other cations. Root growth in the AI-sensitive line was found to be severely inhibited by low activities of AI, even though Ca'+ accumulation was relatively unaffected. In solutions containing the same activity of the AI3+ and Ca2+ ions as above, but also including either 3.0 mM Mg'+, 3.0 mM SI'+, or 30 mM Na+, growth improved, whereas 45Ca2+ accumulation was significantly decreased. Since most of the 45Ca2+ accumulated by roots during short-term treatments will reside in the apoplasm, these results indicate that displacement of Ca2+ from the apoplasm by AI cannot account for the AI-induced inhibition of root growth and, therefore, do not support the Ca2+-displacement hypothesis for AI toxicity. We also show that total accumulation of AI by root apices is greater in the AI-sensitive genotype than the AI-tolerant genotype and suggest that cation amelioration of AI toxicity is caused by the reduction in AI accumulation.Trivalent cations are generally harmful to plants. AI toxicity has attracted particular attention because its prevalence in acid soils can severely limit crop and pasture production. One of the first symptoms of stress is the inhibition of root growth, which can begin within hours or minutes, provided the root apex is directly exposed to A1 . A1 is known to affect many cellular functions, and determining which one of these interactions is the primary cause of toxicity continues to be an important goal (Haug, 1984; Haug and Caldwell, 1985;Taylor, 1988;Kochian, 1995). These investigations often require reliable estimates of AI uptake into the symplasm, but the capacity for the cell wall to accumulate high concentrations of cations makes the resolution of apoplasmic and symplasmic fractions difficult (Dainty and Hope, 1959; Zhang and Taylor, 1990; Reid and Smith, 1992). Some research indicates that A1 can readily cross the plasma membrane (Lazof et al., 1994) and that a large proportion of the A1 in roots resides in the symplasm (Tice et al., 1992; see Taylor,