Retinal Axonal Injury And Oxidative Stress Are Acute Characteristics Of Experimental Traumatic Blast Injury

Abstract

Purpose: : To characterize presence of axonal damage and oxidative stress in retinas exposed to traumatic blast injury (TBI).

Methods: : Healthy adult C57/Bl6 mice were exposed to a blast wave (137 kPa) using a custom built blast chamber. Axonal injury was characterized by evaluating protein expression of beta-amyloid, while possible presence of oxidative stress changes was evaluated by observing pattern of protein expression for inducible nitric oxide synthetase (iNOS) and 4-hydroxy-trans-2-nonenal (4-HNE) by immunohistochemistry.

Results: : One hour post blast injury beta amyloid immunoreactivity was significantly increased in retinas of animals exposed to traumatic blast injury when compared to control (healthy) eyes: ctrl=0.4+0.11 (mean+SEM, n=20); TBI=1+0.2 (n=10), p=0.03 (Unpaired t-test). Evaluation of the 4-HNE (marker for oxidative stress and lipid peroxidation) showed significantly increased immunoreactivity in retinas of TBI animals compared to healthy controls: ctrl=0.0000125+0.00000025 (mean+SEM, n=4); TBI=0.66+1.8 (n=12), p=0.04 (Unpaired t-test). Evaluation of iNOS expression showed a trend toward increased immunoreactivity in TBI injured eyes (0.91+0.49, n=12), when compared to control eyes (0.57+0.16, n=21), however difference was not statistically significant (p=0.08).

Conclusions: : Blast-induced injury results in retinal axonal damage and increased oxidative stress in early periods post injury. Therapeutic strategies targeting oxidative stress may decrease neuronal damage and long term neurological and visual consequences in patients suffering from the blast injury.

Keywords: ganglion cells • oxidation/oxidative or free radical damage • trauma