RENAL CORTICAL MITOCHONDRIA ARE THE SOURCE OF OXYGEN-FREE RADICALS ENHANCED BY GENTAMICIN

Rat renal cortical mitochondria were isolated from Wistar male rats we ighing 80 to 120 g to investigate whether the source of oxygen free ra dicals was renal cortical mitochondria enhanced by gentamicin. In rena l cortical mitochondria with or without the addition of gentamicin, DM SO, DFO, CAT SOD, and MT1 were added separately, then incubated at 37 degrees C for 90 min. Superoxide anions and hydroxyl radicals were the n determined. The results showed that superoxide anions and hydroxyl r adicals generated in mitochondria were enhanced by the addition of in vitro gentamicin (12.4 mg/mL) when compared to those without the addit ion of gentamicin. Dimethylsulfoxide (DMSO), catalase (CAT), and defer oxamine (DFO) significantly inhibited hydroxyl radicals enhanced by ge ntamicin, but superoxide dismutase (SOD) and metallothionein-1 (MT1) d id not. SOD significantly inhibited the production of superoxide anion s. Our data indicated that renal cortical mitochondria are the source of oxygen free radicals and that production is enhanced by gentamicin. This provides more insight on the pathogenetic role of hydroxyl radic als and superoxide anions in gentamicin-induced nephrotoxicity in vitr o.