Effect of Amifostine on Lipid Peroxidation Caused by Cisplatin in Rat Kidney

Cisplatin, a heavy metal complex, is one of the most active drugs used in a variety of certain tumors, including lung, head and neck, ovary, testis, bladder and refractory lymphoma 1. Despite beneficial outcome for some patients, cisplatin treatment has various side effects—especially renal, neurological and ototoxicity 2,3. Tubular damage is the primary expression of renal toxicity from cisplatin. Cisplatin induced renal toxicity can be associated with considerable morbidity 4. The protective activity of amifostine against the tissue damaging effects of cytotoxic agents is well known 5,6. The mechanism of its protective effects are understood. Chemotherapy or radiotherapy kills cells by chemically altering DNA either by ionisation of DNA or by production of highly reactive, diffusable free radicals generated by ionisation of other cellular constituents. Endogen thiols and their ions react with both free and chemical or irradiationinduced DNA free radicals and may increase cell survive if the interactions occur prior to DNA damage or fixation and the effect produced by thiol oxidation reactions. Amifostine is also effective in reducing cisplatin-induced nephrotoxicity 2,6. Journal of Chemotherapy Vol. 13 n. 3 (337-339) 2001