Oxidative Stress of Diethylnitrosamine on the Functions of Kidney in Male Rats and Effective Role of Rutin and/or Selenium

Abstract

Diethylnitrosamine (DENA), one of the most important environmental carcinogen, causes generation of reactive oxygen species resulting in oxidative stress. The present study was designed to examine the ability of rutin (Ru) and selenium (Se), naturally occurring antioxidants, to attenuate DENA-induced nephrotoxicity in adult albino rats. Administration of DENA at a dose level of 200 mg/kg b.wt. to male rats for three times a final week significantly elevated the levels of serum creatinine, uric acid, urea, cortisol, potassium (K), and lactate dehydrogenase( LDH) activity which indicate injury to the kidney function. Also, the tumor necrosis factor- alpha TNF-α increased in serum. On other hand, DENA decreased renal glutathione (GSH) content, glutathione-S-transferase (GST) and superoxide dismutase (SOD). While, DENA induced lipid peroxidation as indicated by markedly increased of malondialdehyde (MDA). DENA intoxication also induced marked alterations in most of the renal tubules including cell depletion and tubular atrophy. Ru 30 mg/kg b.wt. and Se 0.5 mg/kg b.wt orally for 21 days administered 1h before DENA ameliorated the biochemical toxicity induced by DENA, in the kidney. This was evidenced by a significant reduction in serum creatinine, uric acid, urea, cortisol and LDH activity, K and a significant restoration in Na, GSH, GST and SOD. These results indicate that Ru and Se have a protective effect against DENA-induced damage to kidney. This reflects the beneficial role of Ru and Se in treatment of renovascular hypertention and congestive kidney failure.