Abstract

The mechanism by which subthreshold/non-effective doses or concentrations of potassium dichromate (K 2Cr 2O 7) potentiate the effect of moderately effective dose/concentrations of mercuric chloride (HgCl 2) on renal organic ion transport is not understood. To investigate this effect, the rate of excretion of mercury from the intact animal and the renal and hepatic accumulation and subcellular distribution of mercury within kidney cortex following pretreatment or in vitro exposure to K 2Cr 2O 7 were undertaken. Coincidental administration of K 2Cr 2O 7 had no significant effect in altering the rate of excretion of labeled mercury. Organ distribution showed time dependence; however, the presence of K 2Cr 2O 7 did not increase renal mercury concentrations. In fact, significantly less mercury was found at 4 h in the kidneys of rats receiving both metal salts. Subcellular distribution of labeled mercury ( 203Hg) was also not significantly altered by the presence of K 2Cr 2O 7, although the distribution patterns for in vitro exposure and pretreated tissues were different. These studies show that K 2Cr 2O 7 does not produce alterations in urinary elimination, organ distribution or subcellular distribution of mercury.

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