In the oyster Crassostrea virginica the gill was a primary organ for accumulation of Cd from sea water. Gill Cd concentrations measured after 2 weeks of exposure increased as seawater Cd concentrations increased from 0.03 (the control) to 200 μg Cd · liter−1. Both the cytosolic and particulate fractions of gill tissues were involved in sequestering Cd. The cytosolic Cd was bound mainly to metallothionein (MT), which was most effective at binding Cd at the exposure of 50 μg Cd ·liter−1. The relative importance of binding to the particulate fraction was greatest at the lower exposure of 10 μg Cd · liter−1, at which the amount of Cd bound to MT was relatively low, and at the higher exposure of 200 μg Cd · liter−1, at which the capacity for metallothionein to bind Cd appeared to have been exceeded. Gills excised from oysters exposed continuously to 50 μg Cd · liter−1 for up to 24 days were used in a kinetic analysis of the influence of MT induction on intracellular Cd distribution. Short‐term 109Cd‐uptake experiments at this concentration indicated that MT was induced between 1 and 4 days of exposure. Increased binding rates of Cd to MT were attributed to induction of MT and associated with decreased binding to structures in the particulate and to high‐ and low‐molecular‐weight cystolic fractions. The Cd‐binding rates of the different compartments were ranked as MT > particulate fraction > high‐molecular‐weight cytosolic molecules > low‐molecular‐weight cytosolic molecules once MT was induced. The high Cd‐binding rates for MT coupled with the low turnover rates for MT‐bound Cd indicated that MT was the compartment that governed the dynamics of Cd in the whole gill. The intracellular distribution of Cd could be explained on the basis of competitive binding of Cd to intracellular ligands with varying Cd affinities.
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Roesijadi et al. (1989) studied this question.
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