RESISTANCE OF RAT-KIDNEY MITOCHONDRIAL-MEMBRANES TO OXIDATION-INDUCEDBY ACUTE IRON OVERLOAD

The effect of iron-overload on rat kidney was studied after a single i njection of iron-dextran. Total iron content in kidney and isolated ki dney mitochondria was markedly elevated over control values. To assess mitochondrial damage by iron overload, succinate-cytochrome c reducta se and NADH-cytochrome c reductase activities as well as the rare of s uccinate-dependent hydrogen peroxide generation were measured. None of these activities were significantly affected by acute iron overload. The net content and the rate of TBARS (thiobarbituric acid reactive sp ecies) formation in kidney homogenates from iron-treated rats was sign ificantly higher than that of control animals. Total superoxide dismut ase activity in the homogenates from iron overloaded kidney was decrea sed by 26%, as compared to controls. Catalase, glutathione peroxidase, and Mn-superoxide dismutase activities were not affected by the treat ment. The content of alpha-tocopherol was consistently decreased in wh ole kidney homogenates (-31%), mitochondria from kidney medulla (-31%) and cortex (-34%), from iron-overloaded rats. Our data suggest that i ron dextran treatment does not affect kidney integrity, even though in creases in lipid peroxidation occur. Vitamin E appears to be effective in controlling iron-dextran dependent radical generation in kidney.