Abstract
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.
Keywords
animal model - blast-induced-traumatic brain injury - neurodegeneration - oxidative
stress - prolidase
