چکیده (انگلیسی):

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-a) 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-a content and MPO activity
while vitamin E reduced TNF-a 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.