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.