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Role of Lipid Peroxidation in Hg-induced Acute Renal Failure

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KMID : 0647819990220020137
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Abstract

This study was undertaken to determine if N,N-diphenyl-phenylenediamine (DPPD), an potent antioxidant, has a protective effect against HgClz-induced acute renal failure in rabbits. Rabbits received subcutaneous injection of 10 mg/kg IlgClz.
In experiments for DPPD effect, rabbits received intraperitoneally DPPD at a dose of 0.5 g/kg 24 hr before 119Cl2 injection. HgClz treatment induced an increase in serum creatinine levels and a reduction ion glomerular filtration rate, which were accompanied by an increase in fractional excretion of Na+.
These results show that HgClz resulted in toxic acute renal failure. DPPD significantly decreased the increase in urine flow and the reduction in glomerular filtration rate.
DPPD pretreatment also decreased the increased fractional excretion of Na¢¥. The p-aminohippurate uptake by renal cortical slices was inhibited by HgQ-) injection, which was prevented by DPPD. IgCi2 injection caused an increase in lipid peroxidation, and this effect was significantly prevented by DPPD.
These results indicate that the generation of reactive oxygen species plays an important role in HgClz-induced acute renal failure and the protective effect of DPPD is due to inhibition of lipid peroxidation.
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