Biochemical basis of secondary injury following neurotrauma

ABSTRACT

Primary trauma to the nervous tissue initiates a cascade of cellular and molecular events that promote continued tissue damage for an extended period following the initial injury. Oxidative stress mediated injury is an important component of secondary neuronal damage. In an attempt to explore the biochemical origin of oxidative stress associated with secondary injury we studied certain markers of oxidative stress and antioxidants in animal models of head, spinal cord and sciatic nerve injuries. Adult Wistar rats weighing 180-200g were subjected to concussive head injury, compression-induced spinal cord injury and crush injury to the sciatic nerve. Animals in the different groups were killed at various time intervals and the injured tissues [brain, spinal cord and sciatic nerve] were collected. Tissues were analyzed for markers of oxidative stress malondialdehyde, lipid hydroperoxides, conjugated dienes and myeloperoxidase] and level of antioxidants [glutathione and vitamin E]. Results of this study clearly showed a significant increase in the markers of oxidative stress and depletion of antioxidants following neurotrauma. In conclusion, this study clearly demonstrates a role of oxidative stress in the process of neurodegeneration following neurotrauma