Effect of uric acid on nephrotoxicity induced by mercuric chloride in rats

Paula Durante, Freddy Romero, Mariela Pérez, Maribel Chávez, Gustavo Parra

Research output: Articles / NotesScientific Articlepeer-review

11 Scopus citations


Oxidative stress is an important mechanism in mercury poisoning. We studied the effect of uric acid, a natural and potent reactive oxygen species and peroxynitrite scavenger, in HgCl2-induced nephrotoxicity. Rats were injected with a unique dose of HgCl2(2.5 mg/kg body weight, subcutaneously) and then vehicle (for 3 days, twice daily) or HgCl2(unique dose) and intraperitoneal uric acid suspension (250 mg/kg body weight, twice daily, for 3 days), and then killed at 24, 48 and 72 hours after HgCl2administration (n = 5 for each group). At the end of the experimental study, kidneys and blood samples were taken. Tissues were prepared and examined under light microscopy. Uric acid significantly prevented the increase in plasma levels of creatinine and blood urea nitrogen (BUN); it helped maintain systemic nitrate/nitrite concentration and total antioxidant capacity. Uric acid attenuated the increase of renal lipid peroxidation and it markedly diminished nitrotyrosine signal and histopathological changes as early as 24 hours after HgCl2administration. Uric acid did not prevent a decrease in β-actin signal caused by mercuric chloride, but it promoted a faster recovery when compared to the HgCl2alone group. Our results indicate that UA could play a beneficial role against HgCl2toxicity by preventing systemic and renal oxidative stress and tissue damage.

Original languageEnglish
Pages (from-to)163-174
Number of pages12
JournalToxicology and Industrial Health
Issue number3
StatePublished - Apr 2010
Externally publishedYes


  • acute renal failure
  • mercuric chloride
  • nephrotoxicity
  • oxidative stress
  • uric acid


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