Protective effect of vitamin E and atorvastatin against potassium dichromate-induced nephrotoxicity in rats

Potassium dichromate, a Cr (VI) compound, is the most toxic form of Cr (VI) and has been demonstrated to induce nephrotoxicity associated with oxidative stress in humans and animals. The wide environmental distribution of Cr lead to an increased interest of its toxicity and biological effects. The present study was designed to investigate the protective effect of vitamin E and atorvastatin against potassium dichromate-induced nephrotoxicity in rats. A single injection of potassium dichromate (15 mg/kg) to rats induced renal tubule damage and an increase in the following markers of renal injury 2 days later; blood urea nitrogen and serum creatinine. In addition, potassium dichromate injection increased the following nitrosative and oxidative stress biomarkers in kidney; malondialdehyde (MDA), total nitrate/nitrite (Nox). This was associated with a significant reduction in kidney glutathione (GSH), metallothionein (MT) contents and superoxide dismutase (SOD) activity. Furthermore inflammatory mediators such as myeloperoxidase (MPO) and tumor necrosis alpha (TNF-α) were increased. Renal damaged was also evidenced by the change in the kidney histopathological picture. Two weeks pre-treatment with vitamin E or atorvastatin before dichromate administration markedly improved its toxicity as indicated by reduction of serum urea and creatinine as well as improvement of kidney histopathological changes. Oxidative stress biomarkers such as renal MDA and nitric oxide contents were also decreased. Kidney superoxide dismutase activity was restored after pre-treatment with vitamin E. Furthermore, atorvastatin significantly reduced TNF-α content and MPO activity while vitamin E reduced TNF-α content. It could be concluded that the ability of vitamin E as well as atorvastatin to ameliorate potassium dichromate-induced renal injury was associated with their antioxidant and anti-inflammatory properties.