Abstract

A dose of 156 μmoles/kg of sodium maleate, given subcutaneously, enhanced the excretion of mercury by rats treated with penicillamine. This dose of maleate had no effect on kidney function or urine composition including titratable acidity, nor did it change the urinary excretion of endogenous thiol-containing compounds. The pattern of urinary thiol excretion in penicillamine treated animals was also unaffected. Both in vitro and in vivo measurements showed that maleate did not cause any reduction in the number of protein bound thiol groups in the kidneys, and consequently could not release mercury by replacing the metal at those sites. The possibilities that maleate at this dose level slowly induced an irreversible damage resulting in the increased mercury excretion or that maleate acts by reacting with a few but important thiol groups were also rejected as the maleate effect could be reversed by BAL. The reversal of the maleate effect indicated that maleate and the sites responsible for the effect must form ionic bonds and consequently these sites are not thiol groups.

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