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Mechanisms of copper accumulation and detoxification, and of haemocyanin biosynthesis and catabolism, in aquatic arthropods and molluscs are reviewed. Crustacean haemocyanin transports copper in the blood by sequestering additional copper outside the oxygen-binding centre. Large changes in haemocyanin concentration in crustacean blood during moulting and hyposaline exposure generally reflect extracellular volume adjustments rather than biosynthesis and catabolism. Haemocyanin synthesis in decapod crustaceans is stimulated by hypoxia and, in an amphipod, by parasitization. Starvation causes breakdown of haemocyanin. Haemocyanin synthesis occurs principally in the midgut gland of crustaceans and in fixed blood cells (cyanocytes) that are located in certain tissues. It is hypothesized that cyanocytes provide a local oxygen reserve during circulatory arrest. Haemocyanin synthesis occurs primarily in the branchial glands of dibranchiate cephalopods but in the midgut gland of tetrabranchiates. Connective tissue pore cells are proposed as the site of haemocyanin synthesis in gastropods, although similar cells in cephalopod branchial hearts probably catabolize haemocyanin. Crustacean midgut glands contain copper-metallothioneins and glutathione, which donate Cu(I) to apohaemocyanin and function in detoxification and mineralization of excess copper. The physiological significance of high concentrations of quasi-crystalline haemocyanin within vascular spaces of the prosobranch left kidney, opisthobranch blood gland and cephalopod branchial heart appendage is discussed.

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