Renal Function and Mercury Level in Rats with Mercuric Chloride Nephrotoxicity

Abstract

The levels of Hg++ in different subcellular compartments of rat kidney cortex were determined after a single subcutaneous injection of ²⁰³HgCl₂, 4.7 mg/kg body weight. By 30 min after injection, cortical Hg⁺⁺level was 46.3 ± 6.8 µg/g protein. A maximal cortical Hg^++· value of 429 ± 49 µg/g protein was reached 4 h after injection. Hg⁺⁺associated with the brush border membrane showed a progressive increase during the first 15 h after injection, but at each time interval was significantly less than cortical Hg⁺⁺ The 45-hour values for cortex and brush border were equivalent. No evidence for the presence in plasma or kidney tissue of free Hg⁺⁺ was obtained. Saline loading protected animals against the development of renal failure and resulted in significant lowering of cortical Hg⁺⁺ levels without an effect on blood Hg⁺⁺ concentrations.

Effects of Furosemide Diuresis on Mercuric Chloride-Induced Acute Renal Failure in the Rat

“…In rats, provision of normal saline in place of drinking water has been found to attenuate the development of HgCl2-induced ARF; it has been suggested that chronic saline loading may protect against the nephrotoxic ef fects of HgCl2 by promoting the urinary excretion of mercury and by reducing mercury levels in the renal cortex [16]. In the present study of rats given HgCl2, the urinary excretion of mercury in rats given furosemide might have been greater than that in control rats not given the diuretic.…”

“…In the setting of ARF, an increase in urinary excretion of solute and water induced by administration of a di uretic may flush out tubular debris, decrease intratubular obstruction, and enhance the excretion of nephrotoxins [13][14][15][16], However, these beneficial effects might be coun tervailed by a deleterious effect on renal function of diuretic-induced volume depletion [7], Thus, in patients and animals with ARF, it may be necessary to carefully control volume status in order to consistently observe a beneficial effect of furosemide on renal function. The timing of furosemide administration might also be a critical determinant of its ultimate effect on the course of ARF; administration of furosemide during the early stages of ARF may be more likely to exert a beneficial effect on renal function than its administration late in the course of renal failure [14],…”

Effects of Sodium Intake and Nephrotoxin Dose on Acute Renal Failure in the Young Rat

“…The precise mechanisms by which nephrotoxins such as HgCl2 and UN induce ARF in experimental animals remain to be elucidated (10,14,16,23,34,35). The critical target sites for these nephrotoxins as well as their modes of delivery to these sites remain conjectural (23,35,37).…”

“…The critical target sites for these nephrotoxins as well as their modes of delivery to these sites remain conjectural (23,35,37). Moreover, the relationships of the various enzymatic, biochemical, structural ' and functional derangements that occur after nephrotoxin administration are still unclear (23,25,26,35,37). Decreased renal blood flow, tubular obstruction, and backleak of filtrate have all been reported to play major roles (9, 11, 14-17, 27, 34, 35, 37).…”

“…The mechanism iinot know; Both long-term and short-term changes in Na intake and/or excretion are effective in mature rats, and the protective effects are independent of changes in the activity of the reninangiotensin system (5,7,8,10). It has been suggested that a state of sustained solute diuresis may increase the rate of nephrotoxin elimination and minimize prolonged tubular injury and obstruction (5,7,11,23,26,27,35). Whatever the mechanism, that the protective effect can be achieved in the young may have important clinical implications.…”