Superoxide dismutase with prolonged in vivo half-life inhibits intravascular hemolysis and renal injury in burned rats.

Although superoxide radicals and related metabolites have been postulated to underlie the pathogenesis of burn injury, critical evidence supporting this hypothesis is lacking. To test whether superoxide radicals play critical roles in burn injury, the effect of a superoxide dismutase (SOD) derivative (SM-SOD) was tested on intravascular hemolysis and renal tubular injury in rats subjected to burn shock. Within 3 hours after a given full-thickness burn of approximately 24% of body surface area, plasma levels of lipid peroxides increased significantly with concomitant increase in intravascular hemolysis. Histological examination showed a marked deposition of hemoglobin-like casts in renal tubules of the burned rats. Intravenous administration of SM-SOD (10 mg/kg) 30 minutes before the burn injury significantly inhibited the increase of plasma lipid peroxides and the occurrence of intravascular hemolysis. SM-SOD also inhibited the deposition of casts in renal tubules. These results indicate that superoxide radicals play critical roles in the pathogenesis of intravascular hemolysis and renal damage induced by burn injury.