The endogenous activity of the neuroprotective enzyme superoxide dismutase (SOD) and the amount of lipid peroxidation in the early phase of experimental spinal cord injury, together with the effects of N-methyl-D-aspartate (NMDA) antagonist CPP and non-NMDA antagonist NBQX on lipid peroxidation were evaluated. The clip compression model was used for the production of a standardized spinal cord trauma. SOD activity and malondialdehyde (MDA) levels--as an indicator of lipid peroxidation--were determined in the injured segment of the spinal cord 30 and 60 min after injury. SOD activity did not change in this period, whereas MDA levels at 30 and 60 min after trauma were significantly elevated. Intrathecal administration of CPP or NBQX 15 min after injury produced statistically significant reductions in MDA elevation 60 min after injury. NBQX was found to be more effective than CPP. These results demonstrated that intrathecal local application of excitatory amino acid receptor antagonists can protect the spinal cord from secondary damage caused by the generation of lipid peroxides in experimental spinal cord injury.