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.