Complexing activity of 2,3-dimercapto-1-propanesulfonate and its disulfide auto-oxidation product in rat kidney.

The complexing activity of 2,3-dimercapto-1-propanesulfonate (DMPS) was examined in vivo and in the isolated perfused rat kidney. Intravenous infusions of the sulfhydryl form of DMPS into rats pretreated with HgCl2 resulted in a dose-dependent increase in the urinary excretion of mercury and a decrease in the retention of mercury in kidney. A 120-min infusion of 2 mg sulfhydryl DMPS.min-1.kg body wt-1 resulted in excretion of 76% of the mercury body burden of which greater than 90% was removed from kidney. The disulfide auto-oxidation product of DMPS significantly increased the urinary excretion of mercury in the rat, but its effect was less than that of an equivalent dose of sulfhydryl DMPS. The presence of disulfide DMPS or 3:1 mixtures of sulfhydryl DMPS and disulfide DMPS in the perfusate increased the excretion of mercury and induced a loss of mercury from the cortex and outer medulla in the isolated perfused rat kidney. Thus both the disulfide and sulfhydryl forms of DMPS can act directly on the kidney to accelerate the excretion of mercury. This is consistent with previous observations of the ability of the kidney to reduce disulfide DMPS to sulfhydryl DMPS.