INCREASED URINARY CALCIUM AND MAGNESIUM EXCRETION IN RATS INJECTED WITH MERCURIC-CHLORIDE

Mercuric chloride (HgCl2) is a classic nephrotoxic agent. While it is well established that HgCl2 can induce metallothionein synthesisin the kidney and also cause damage to the pars recta region of the renal tubule, the urinary losses of essential elements like calcium (Ca) and magnesium (Mg) probably related to this process, have not been described. In this study, calcium, magnesium, metallothionein (MT), as well as sodium (Na) and potassium (K) in urine, kidney cortex and liver were measured in male Wistar rats after two daily injections of HgCl2 (0.5 or 1.0 mg Hg/kg body weight intraperitoneally). As compared with controls, there was a significant 3-4-fold increase in calcium excretion which reached its maximum at 8-12 and 32-36 hr after treatment with 1.0 mg Hg/kg. Urinary magnesium excretion was also increased in a similar way as the calcium excretion. At 12-16 hr, urinary magnesium in the 1.0 mg Hg/kg dose group was 3.4 times higher than that of the controls. Urinary MT level in HgCl2 treated rats was much higher than that in the controls, the maximum excretion was between 24-28 and 32-36 hrs preceeded by the peak of Hg in urine. Na and K concentrations in urine decreased significantly in rats treated with HgCl2. The present study thus demonstrates that increases of urinary calcium and magnesium excretion are early toxic effects of HgCl2 on the kidney. It gives support to the hypotheses implying these ion imbalances in the mechanism of elicitation of renal toxicity by mercury. These findings are also of interest because they indicate the possibility that perturbations of Ca and Mg metabolism as a result of environmental (including occupational) mercury exposure might occur; such ion imbalances might subsequently increase risks of adverse health effects.