Some patients with an acute spinal cord injury (SCI) can immediately become paraplegic following the trauma. On the other hand, some patients vvith an incomplete trauma can be deteriorated by time as a result of the vvorsening pathology on the spinal cord. Consequently, great amount of sensorimotor functions are lost because of this delayed secondary (auto-destructive) response since many etiological factors are responsible for auto-destructive progression. A significant number of treatments are developed in the literatüre.

İn this study, the effects of Deferoxamine (DFO) which inhibits iron dependent lipid peroxidation were investigated on 64 rats, equally divided into 2 subgroups, Control (C) and Treatment (T). Extradural clip compression at the thoracic 7 level vvas selected as a trauma model. 15 minutes before the trauma, 100 mg/kg DFO and same dosage of serum physiologic vvas injected intravenously to T and C subgroups respectively. Follovving the trauma, at the first, 30th, 60th and 120th minutes biologic activity vvas stopped vvith Iiquid nitrogen. Lipid peroxidation and the effects of the treatment vvere determined biochemically by the assessment of malonic dialdehid through the tiobarbituric acid test.

DFO reduced lipid peroxidations at the 60th and 120th minutes. This reduction vvas particularly more definite at the first 60 minutes. This study concludes that DFO can be effective on the secondary auto-destructive processes after an experimental SCI.

Keywords: Deferoxamine, experimental spinal cord injury, iron chelates, lipid peroxidation, rat