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Aluminium is the third most abundant element in the lithosphere and yet no biological function has been elucidated. The ubiquity and pH-dependent chemical speciation of aluminium provides multiple routes of exposure to organisms, inducing neurotoxicity, tissue necrosis and organelle dysfunction. However, many studies of aluminium toxicity lack consideration of the speciation and relevant concentration of aluminium and the route of exposure. The aim of this thesis was to examine the accumulation, distribution, excretion and toxicity of aluminium following a common route of exposure (ingestion) at a concentration likely to be encountered by the model organism (freshwater crayfish, Pacifastacus leniusculus) in the wild. Crayfish are sediment dwelling omnivorous crustaceans distributed worldwide and as such are vulnerable to multiple routes of aluminium exposure. They play a central role in aquatic food webs and are becoming increasingly popular for human consumption, raising concern about food chain transfer. Crayfish were fed aluminium chloride-spiked artificial food pellets for either 20 days, 28 days + 10 day aluminium-free clearance period, or 22 weeks + 4 week aluminium-free clearance period. In addition, systemic administration of aluminium citrate was undertaken to draw comparisons with previous mammalian work and compare the two routes of exposure. Tissue distribution and accumulation was measured in the gills, hepatopancreas, flexor muscle and antennal gland. Stress and tissue damage were analysed using biochemical and histopathological techniques. Behavioural toxicity tests and measurements of the neurophysiological parameters of the crayfish medial giant neuron were used to assess aluminium-induced neurotoxicity. In vitro neurotoxicity tests with aluminium chloride were also carried out on isolated nerve tissue to assess the suitability of in vitro studies. The key site of aluminium accumulation following ingestion was the hepatopancreas. Excretion was observed via the gills, antennal glands (in the urine) and hepatopancreas (for incorporation into the faeces). However, physiological consequences such as tissue damage, inflammation and altered neuronal activity were observed and persisted even after cessation of aluminium ingestion. Consequently there are implication for crayfish fitness and survival, the aquatic food web and human toxicity following ingestion of aluminium.

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