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

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 HgCl( 2)-induced nephrotoxicity. Rats were injected with a unique dose of HgCl(2) (2.5 mg/kg body weight, subcutaneously) and then vehicle (for 3 days, twice daily) or HgCl(2) (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 HgCl(2) administration (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 HgCl(2) administration. Uric acid did not prevent a decrease in beta-actin signal caused by mercuric chloride, but it promoted a faster recovery when compared to the HgCl(2) alone group. Our results indicate that UA could play a beneficial role against HgCl(2) toxicity by preventing systemic and renal oxidative stress and tissue damage.