The effect of deferoxamine on SOD and histopathological changes following experimental spinal cord injury

Background: Primary traumatic spinal cord injury is defined as the injury occurring at the time of the trauma. The metabolic and biochemical processes lead to the secondary trauma in the following hours after the primary trauma. Free radicals and ischemic reperfusion injury are two factors which play role in secondary injury.An iron chelating agent deferoxamine has a high affinity for iron and known as antioxidant agent. Deferoxamine has treatment effect on secondary injury mechanisms by binding free iron ion. It is known to cross the cell membrane and blood brain barrier because of low molecular weight. This study based on these effects of deferoxamine and free radicals injury as one of the mechanisms causing secondary spinal cord injury.Methods and Materials: The experimental spinal cord injury model was applied on 26 rats. In control group I 10 rats were sacrificed to provide normal spinal cord histopathology and biochemical baseline values. In group II 6 rats underwent six segment laminectomy and spinal cord injury was produced by exstadural compression of the exposed cord by aneurysm clip. Same procedures were performed in 10 rats in group III, but they also received 100mg/kg/day intraperitoneal injection of deferoxamine. Group II and III were sacrificed at 48 hours after the trauma. The effect of deferoxamine on superoxide dismutase and histopathological findings were studied.Results: As a result superoxide dismutase values were found to decrease significantly when compared to the trauma group. The histopathological evaluation reveled the preservation of spinal cord structure in the treatment group.Conclusion: Results showed that deferoxamine, might reduce secondary injury in damaged rat spinal cord tissue, by a possible mechanism of decreasing the production of free radicals.