The suitability of gallium as a substitute for aluminum in tracing experiments.

Aluminum is a toxic metal whose complex aquatic chemistry, mechanisms of toxicity and trophic transfer are not fully understood. The only isotope of Al suitable for tracing experiments in organisms-(26)Al-is a rare, costly radioisotope with a low emission energy, making its use difficult. Gallium shares a similar chemistry with Al and was therefore investigated as a potential substitute for Al for use in aquatic organisms. The freshwater snail, Lymnaea stagnalis was exposed to either Al or Ga (0.0135 mM) under identical conditions for up to 40 days. Behavioural toxicity, metal accumulation in the tissues, and sub-cellular partitioning of the metals were determined. Al was more toxic than Ga and accumulated to significantly higher levels in the soft tissues (P < 0.05). The proportion of Al in the digestive gland (DG; detoxificatory organ) relative to other tissues was significantly lower than that of Ga (P < 0.05) from day 14 onwards. There were also differences in the proportions of Al and Ga associated with heat stable proteins (HSPs) in the digestive gland, with significantly more HSP present in the DGs of snails exposed to Al, but significantly less Al than Ga associated with the HSP per unit mass protein present. From this evidence, we conclude that Ga may be of limited use as a tracer for Al in animal systems.

Avoidance of aluminum toxicity in freshwater snails involves intracellular silicon-aluminum biointeraction.

Silicon (Si) ameliorates aluminum (Al) toxicity to a range of organisms, but in almost all cases this is due to ex vivo Si-Al interactions forming inert hydroxyaluminosilicates (HAS). We hypothesized a Si-specific intracellular mechanism for Al detoxification in aquatic snails, involving regulation of orthosilicic acid [Si(OH)4]. However, the possibility of ex vivo formation and uptake of soluble HAS could not be ruled out Here we provide unequivocal evidence for Si-Al interaction in vivo, including their intracellular colocalization. In snails preloaded with Si(0H)4, behavioral toxicity in response to subsequent exposure to Al was abolished. Similarly, recovery from Al-induced toxicity was faster when Si(OH)4 was provided, together with rapid loss of Al from the major detoxificatory organ (digestive gland). Temporal separation of Al and Si exposure excluded the possibility of their interaction ex vivo. Elemental mapping using analytical transmission electron microscopy revealed nanometre-scale colocalization of Si and Al within excretory granules in the digestive gland, consistent with recruitment of Si(OH)4, followed by high-affinity Al binding to form particles similarto allophane, an amorphous HAS. Given the environmental abundance of both elements, we anticipate this to be a widespread phenomenon, providing a cellular defense against the profoundly toxic Al(III) ion.