Protection against mercuric chloride by nephrotoxic agents which do not induce thionein
Tandon, S.K.; Magos, L.; Cabral, J.R.
Toxicology and Applied Pharmacology 52(2): 227-236
1980
ISSN/ISBN: 0041-008X PMID: 7361322 Document Number: 161461
Kidney damage caused by the i.p. administration of 1.1 mg/kg Hg given as HgCl2 was less marked in 7 wk old male rats when Hg was given 7 days after the administration of 1 of the following nephrotoxic agents: 20 mg/kg sodium chromate, 100 mg/kg p-aminophenol, or 500 mg/kg sodium maleate, or 14 days after the injection of 4.0 mg/kg uranyl acetate. All 4 nephrotoxic agents were given in sufficient doses to cause renal damage. In the first 3-4 days after the administration of the nephrotoxic agents, they increased the urinary excretion of alkaline phosphatase, glutamic oxaloacetic transaminase and lactic dehydrogenase and caused widespread necrosis in the proximal tubular cells. In the first 24 h after the injection of Hg, the urinary excretion of the 3 enzymes tested was lower in pretreated than in nonpretreated rats. Tubular cell necrosis was also less extensive in pretreated than in nonpretreated rats. Tubular cell necrosis was also less extensive in pretreated than in nonpretreated rats and calcification could be seen 10 days after Hg only in the kidneys of the nonpretreated rats. The decreased susceptibility of regenerating kidneys to the tubulotoxic effect of HgCl2 is a general phenomenon which is unrelated to the renal concentration of metalothionein or change in renal Hg uptake.