Clinica chimica acta; international journal of clinical chemistry · 2007
Vitamin C attenuates potassium dichromate-induced nephrotoxicity and alterations in renal brush border membrane enzymes and phosphate transport in rats.
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Fatima Sabiha, Mahmood Riaz
Аннотация
BACKGROUND: Exposure to chromium compounds can result in nephrotoxicity. The administration of potassium dichromate (K(2)Cr(2)O(7)), a hexavalent chromium compound, results in impairment in functions of renal brush border membrane (BBM).
METHODS: The effect of vitamin C (ascorbic acid) on K(2)Cr(2)O(7)-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, K(2)Cr(2)O(7) alone and vitamin C plus K(2)Cr(2)O(7). Nephrotoxicity was evaluated by urea and creatinine levels in the serum. Anti-oxidant status was evaluated in kidney homogenates.
RESULTS: A single dose of K(2)Cr(2)O(7) (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 K(2)Cr(2)O(7). It greatly ameliorated the K(2)Cr(2)O(7)-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.
CONCLUSIONS: Vitamin C is an effective chemoprotectant against K(2)Cr(2)O(7)-induced acute renal failure and dysfunction of the renal BBM in rats.
METHODS: The effect of vitamin C (ascorbic acid) on K(2)Cr(2)O(7)-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, K(2)Cr(2)O(7) alone and vitamin C plus K(2)Cr(2)O(7). Nephrotoxicity was evaluated by urea and creatinine levels in the serum. Anti-oxidant status was evaluated in kidney homogenates.
RESULTS: A single dose of K(2)Cr(2)O(7) (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 K(2)Cr(2)O(7). It greatly ameliorated the K(2)Cr(2)O(7)-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.
CONCLUSIONS: Vitamin C is an effective chemoprotectant against K(2)Cr(2)O(7)-induced acute renal failure and dysfunction of the renal BBM in rats.