Ultrastructural and biochemical studies of intracellular metal-binding patterns in kidney tubule cells of the scallop Placopecten magellanicus following prolonged exposure to cadmium or copper

Sea scallops Placopecten magellanicus, which had been trawl-collected in late November, 1982 off the Rhode Island, USA coast, were exposed to 20 g of Cd or Cu per liter for a period of seven weeks in a flowing seawater system. Metal analyses of kidneys from both groups indicated uptake of both metals, although the tissue concentrations of Cd declined markedly in the Cu-treated scallops. The ultrastructural appearance of tubule cells of kidneys from Cd-exposed scallops was indistinguishable from controls. In contrast, tubule cells from scallops exposed to Cu showed marked cellular degeneration with loss of concretions. These ultrastructural changes were associated with significant reductions in renal isocitrate dehydrogenase activity in the Cu-treated scallops. Elemental analyses conducted on the kidney concretions and on the cytosolic metal-binding proteins of Cd-exposed scallops showed a 6-to 7-fold increase in Cd content of both these metalsequestering compartments, with concomitant changes in Zn, Mn, and Cu content. Loss of the concretions from Cu-treated scallops precluded analysis of this compartment, but Cu sequestration within cytosolic metal-binding proteins was associated with marked reductions of Zn and Cd from these proteins, suggesting disruption of this cellular mechanism for control of divalent metal cations. These findings support the hypothesis that toxic metal perturbation of normal homeostatic mechanisms that control divalent metal cation bioavailability is important factor in mediating cell injury from these agents.