Effect of ACE inhibitors on cisplatin-induced nephrotoxicity in rats

The effects of captopril and enalapril on cisplatin-induced nephrotoxicity in rats were evaluated. Aqueous solution of either captopril or enalapril was administered orally for 7 days. Cisplatin [15 mg/kg,i.p.] was injected in non-treated rats or with last dose of either captopril or enalapril30 hrs before animal sacrificing. Captopril failed to alter serum urea and creatinine, renal non-protein thiol and malondialdehyde contents. However, enalapril in a high dose [20mg/kg] increased serum creatinine, non-protein thiol. Cisplatin increased serum urea and creatinine levels, renal non-protein thiol and malondialdehyde content. Pretreatment with captopril decrease the effects of cisplatin on serum urea, renal RNA and DNA and. non-protein thiol. In contrast, enalapril potentiated the effects of cisplatin. It is concluded that the protective effect of captopril is a function of sulfhydryl group. Further studies are suggested in determining the role of thiol compounds as a basis for cisplatin-induced nephrotoxicity and its prevention

Cytological effects desferrioxamine in somatic cells of Swiss albino mice

Desferroxamine an iron chelator, has been shown to be ineffective in increasing the frequency of micronuclei in bone marrow cells of mice on acute and sub - acute treatment. However, a significant mitodepressive effect is produced at the higher dose on sub - acute treatment. The mito - depressive potentials of DFO may be either due to the disproptionate ratio of Fe2+/Fe3+ which is known to stimulate lipid peroxidation or due to total chelation of iron resulting in bone narrow depression and anemic condition