Vitamin C attenuates potassium dichromate-induced nephrotoxicity and alterations in renal brush border membrane enzymes and phosphate transport in rats

BackgroundExposure to chromium compounds can result in nephrotoxicity. The administration of potassium dichromate (K2Cr2O7), a hexavalent chromium compound, results in impairment in functions of renal brush border membrane (BBM).MethodsThe effect of vitamin C (ascorbic acid) on K2Cr2O7-induced nephrotoxicity, changes in BBM enzymes, Pi transport and the anti-oxidant status of rat kidney were studied. Animals were divided into 4 groups and were intraperitoneally given saline (control), vitamin C alone, K2Cr2O7 alone and vitamin C plus K2Cr2O7. Nephrotoxicity was evaluated by urea and creatinine levels in the serum. Anti-oxidant status was evaluated in kidney homogenates.ResultsA single dose of K2Cr2O7 (15 mg/kg body weight) resulted in an increase of serum urea nitrogen and creatinine levels, increase in lipid peroxidation and decrease in total sulfhydryl groups. However, prior treatment with a single dose of vitamin C (250 mg/kg body weight) protected the kidney from the damaging effects of K2Cr2O7. It greatly ameliorated the K2Cr2O7-induced nephrotoxicity and reduction in Pi transport, activities of catalase, Cu–Zn superoxide dismutase and BBM enzymes. This was accompanied by decrease in lipid peroxidation and recovery of sulfhydryl content of renal cortex.ConclusionsVitamin C is an effective chemoprotectant against K2Cr2O7-induced acute renal failure and dysfunction of the renal BBM in rats.