Effect of prolonged saline loading on HgCl2-induced renal tubular damage.
Male Porton-Wistar rats, 32 weeks old, were given i.p. one of the following doses of HgCl2; 0.5, 1.0 or 1.5 mg Hg/kg. In the preceding 4-week period and throughout the experiment the animals had free access to either tap water or 1.0% saline. The urinary excretion of alkaline phosphatase measured in urine samples, collected during the first 24 h after treatment with mercury, indicated that chronic saline loading significantly attenuated tubular damage caused by 0.5 mg or 1.0 mg Hg/kg, but not by 1.5 mg Hg/kg. Tubular necrosis 12 and 24 h after mercury was also less severe and extensive in saline than in tap water-drinking rats. This difference was still noticeable 4 days after mercury treatment in rats dosed with 0.5 mg Hg/kg, but death in the two higher dose groups prevented further pair-to-pair histological comparison. At the selected dose levels chronic saline loading did not decrease renal mercury content at 12 or 24 h and therefore protection was not associated with decrease in renal mercury uptake. The experiment indicates that chronic saline drinking, which at higher doses attenuates HgCl2-induced acute renal failure but not tubular necrosis, is able to moderate the severity of tubular necrosis when the dose of HgCl2 is as low as 0.5 mg Hg/kg. This protective effect diminishes as the dose is increased.
D058186:Acute Kidney Injury / Q000473:pathology*; D000469:Alkaline Phosphatase / Q000652:urine; D000818:Animals; D004305:Dose-Response Relationship, Drug; D007683:Kidney Tubular Necrosis, Acute / Q000139:chemically induced / Q000473:pathology*; D008297:Male; D008627:Mercuric Chloride; D008628:Mercury / Q000652:urine; D051381:Rats; D011919:Rats, Inbred Strains; D012965:Sodium Chloride / Q000494:pharmacology*; D013997:Time Factors
D012965:Sodium Chloride; D008627:Mercuric Chloride; D000469:Alkaline Phosphatase; D008628:Mercury