Therapeutic Efficacy of Selenium in Management of Hyperhomocytenemia in Cisplatin-Induced Nephrotoxicity

Abstract

Nephrotoxicity is a prominent cause of global of injury and mortality. The aim here is to investigate the therapeutic role of selenium in treatment of cisplatin-induced experimental nephropathy. Animals were classified into four groups including cisplatin group in which animals were injected (intraperitoneal) with a single dose of cisplatin, while treated group in which rats injected with cisplatin and then received selenium (0.5 mg /k.g.b.w. / day) orally for ten days , control group , and selenium group in which healthy rats received selenium in a dose of 0.5 mg /k.g.b.w. / day , orally for ten days .After the experimental period, samples (blood and kidney tissues) were collected from each rat to estimate different biochemical and histological parameters using different techniques. Cisplatin significantly increased serum creatinine and urea comparing to control. However, reduction in catalase antioxidant enzyme was recorded in nephrotoxic rats, while marked increase in lipid peroxide (MDA), Advanced Oxidant Protein Product (AOPP), interleukin-1β(IL-1β), ceramide, tumor necrosis factor –α (TNF–α), metalloproteinase -9 (MMP-9)and homocysteine (Hcy) levels was detected as compared to control. Histopathological investigation revealed necrobiotic changes and deterioration in the lining tubular epithelium and tubular cystic dilatation at the cortex and inflammatory cells between the degenerated tubules. Treatment with selenium showed improvement in histopathological picture and corrective effects in all biomarkers under investigation. Nephrotoxicity induced by csplatin in rats is associated with remarkable elevation of oxidative stress, inflammatory markers, and renal histopathological lesions. While, the therapeutic effect of selenium (Se) may be attributed to` the alleviation of ROS-mediated apoptosis. These current results indicated that Se may be offer a promising dietary supplement against nephrotoxicity.