RESUMEN
In order to elucidate the mechanisms of nickel [Ni+2] induced renal oxidative damage in rats, the ability of renal cortical mitochondria [RCM] to generate reactive oxygen species was investigated in vitro. The generation of superoxide anion radical [O2-] was assessed by the reduction of ferricytochrome c assay. Hydrogen peroxide [H2O2] was monitored by phenol red horseradish peroxidase technique and hydroxyl radicals [OH] generation was monitored by deoxyribose degradation assay in rat RCM incubated with Ni+2. In RCM with or without the addition of Ni+2, catalase, superoxide dismutase [SOD], salicylate, mannitol, phenylalanine, arginine, dimethyl thiourea [DMTU], urea, albumin and desferrioxamine [DFO] were added separately, then incubated at 37C for 90 minutes. The present results indicated that Ni+2 -induced renal oxidative damage is mediated by an accelerated production of reactive oxygen species by RCM