Potassium bromate-induced oxidative damage and nephrotoxicity in rats is ameliorated by vitamin C

Potassium bromate (KBrO3), a widely used food-additive and a major water disinfection by-product, causes severe toxicity in humans and experimental animals. Bromate is considered a probable human carcinogen and a complete carcinogen in animals. We have investigated the potential role of vitamin C in mitigating KBrO3-induced nephrotoxcity. Animals were given KBrO3 alone or after pretreatment with vitamin C and then sacrificed. Blood and kidneys were collected and were used for the analysis of several biochemical parameters. Administration of single oral dose of KBrO3 alone caused nephrotoxicity as evident by elevated serum creatinine (+3-fold) and urea levels (+2.5-fold). Renal lipid peroxidation (+1.5-fold) and protein carbonyls (+2.5 fold) were increased while total sulfhydryl groups (−2.3-fold) and reduced glutathione levels (−1-fold) were decreased suggesting the induction of oxidative stress. The enzymes of renal brush border membrane were inhibited and those of carbohydrate metabolism were altered. There was increase in DNA damage and DNA-protein cross-linking. Treatment with vitamin C, prior to administration of KBrO3, resulted in significant attenuation in all these parameters but the administration of vitamin C alone had no effect. Histological studies supported these biochemical results showing extensive renal damage in KBrO3 alone treated animals and greatly reduced tissue injury in the vitamin C + KBrO3 group. These results show that vitamin C is an effective chemoprotectant against bromate-induced renal damage and could prove to be useful in attenuating the toxicity of this and other related compounds.