Blast-induced traumatic brain injury (TBI) poses a significant threat to individuals exposed to explosive events. We hypothesized that blast-induced neurotrauma is an oxidative stress to brain and hence prolidase (PD) enzyme, which is an antioxidant is recommended; its serum levels are better markers of degree of injury in the acute phase for TBI in a rat blast injury model. Results revealed that PD enzyme activity in the hippocampus showed a slight increase across high, medium, and low blast pressures, but remained lower than the sham group. However, serum PD enzyme activity levels were significantly higher in the blast-exposed groups compared to the sham group. Tau protein levels were significantly elevated in the blast-exposed groups. Longitudinal analysis demonstrated a decline in hippocampal PD activity over time, while tau protein levels progressively increased, suggesting a shift from initial oxidative stress to neurodegeneration. These findings suggest that blast injury triggers oxidative stress and subsequent neurodegenerative processes. The correlation with tau protein levels further supports the involvement of oxidative stress in neurodegeneration. In conclusion, this study provides insights into the underlying pathophysiological mechanisms of blast-induced TBI and highlights the potential utility of PD enzyme activity as a diagnostic marker.

Work discussed in this article was presented in the award paper category at NTSI conference Jaipur August 2023.

*National Institute for Health and Care Research Collaborators, NIHR, Cambridge, UK

Article published online:
29 April 2024

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