RESUMO
Many in vivo and in vitro studies performed mainly in liver have been shown silymarin to be a potent anti-oxidant, and one of the most potent scavengers of hydroxyl radicals. Therefore, it is plausible to expect that it may produce these effects against oxidalive stress consequences induced by gentamicin in the kidney. Evaluation of the protective effect of different doses of silymarin given orally in protecting rats against gentamicin-induced nephrotoxicity. Groups of rats [6 rats each] were pre-treated for 7 days with 250, 500, and l000 mg/kg silymarin and vehicle orally before induction of renal toxicity with gentamicin, and another 6 rats were utilized as controls. The parameters of oxidative stress, malondialdehyde [MDA], and glutathione [GSH] were measured in the serum and kidney tissue homogenate, in addition to serum levels of urea and creatinine. Histopathological examination of stained tissue sections from the kidney was performed; in addition to silymarin level in the kidney tissue homogenate was evaluated using HPLC method. Analysis of data revealed significant amelioration of oxidative stress, experimentally induced in the kidney through lowering MDA and elevation of GSH levels, both in serum and tissue homogenate, associated with significant reduction of serum levels of urea and creatinine, and with positive histological evidences for the protective effect of silymarin which is found to be related to the increase in its renal tissue availability when the oral dose was increased. These findings suggest that, silymarin is effective in preventing gentamicin-induced renal toxicity, which makes it a good candidate for clinical use in this respect