3.5. Lipid peroxidation

Lipids are abundantly found in tissues of CNS and PNS, which indicate that spinal cord is more vulnerable to lipid peroxidation that can lead to lysis of cell membrane [9]. Since free radicals are abundantly present in injury site, increases in their level will eventually lead to lysis of cell membranes via lipid peroxidation. Consequently, mitochondrial dysfunction occurs as a result of oxidative damage and induces calcium overload [20]. The calcium influx causes ion imbalance and excitotoxicity, which is triggered through acute SCI [9]. Additionally, high level of glutamate is released after SCI, which results in increased calcium influx and damage to the spinal cord by stimulating the AMPA and NMDA receptors that induce neuronal death by apoptosis or necrosis [21]. The oligodendrocytes and neurons are susceptible to glutamate excitotoxicity as they express glutamate receptors [3]. Consequently, excitotoxic injury induces axonal demyelination. Additionally, nitrous oxide is involved in glutamate excitotoxic injury [22]. The increased calcium ions level has a major role in the secondary injury mechanism.
