The comparative renotoxicology of phenylmercury and mercuric chloride.
The acute renotoxicity of HgCl2 and phenylmercuric acetate (PhHgAc) was compared at two intraperitoneal dose levels: 0.5 and 1.0 mg Hg/kg. There was no difference in the type of proximal tubular damage caused by the two mercurials, but 1.0 mg Hg/kg as PhHgAc produced approximately the same degree of damage as 0.5 mg Hg/kg as HgCl2. At the selected dose levels only HgCl2, but not PhHgAc increased the urinary excretion of alkaline phosphatase. At 12 and 24 h after PhHgAc the content of mercury was higher in blood and lower in the kidneys and urine than after the administration of equimolar doses of HgCl2. As the difference in the rectal mercury contents of HgCl2 and PhHgAc treated groups declined with time, difference in renotoxicity seems to relate only to renal mercury taken up within 24 h of administration. It is suggested that the slower renal extraction of mercury - as in regenerating kidneys (Tandon and Magos 1980) - was responsible for the lower degree of renotoxicity in phenylmercury treated rats.
D000469:Alkaline Phosphatase / Q000652:urine; D000818:Animals; D007674:Kidney Diseases / Q000139:chemically induced* / Q000473:pathology; D007687:Kidney Tubules, Proximal / Q000473:pathology; D008297:Male; D008627:Mercuric Chloride; D008628:Mercury / Q000097:blood / Q000633:toxicity*; D010662:Phenylmercuric Acetate / Q000633:toxicity*; D010663:Phenylmercury Compounds / Q000633:toxicity*; D051381:Rats; D011919:Rats, Inbred Strains
D010663:Phenylmercury Compounds; D008627:Mercuric Chloride; D000469:Alkaline Phosphatase; D008628:Mercury; D010662:Phenylmercuric Acetate