The oxidative mechanisms of injury-induced damage of neurons
within the spinal cord are not very well understood. We used a
model of T8-T9 spinal cord injury (SCI) in the rat to induce
neuronal degeneration. In this spinal cord injury model, unilateral
avulsion of the spinal cord causes oxidative stress of neurons. We
tested the hypothesis that apurinic/apyrimidinic endonuclease (or
redox effector factor-1, APE/Ref-1) regulates this neuronal
oxidation mechanism in the spinal cord region caudal to the
lesion, and that DNA damage is an early upstream signal. The
embryonic neural stem cell therapy significantly decreased DNAdamage levels in both study groups – acutely (followed up to
7 days after SCI), and chronically (followed up to 28 days after
SCI) injured animals. Meanwhile, mRNA levels of APE/Ref-1
significantly increased after embryonic neural stem cell therapy in
acutely and chronically injured animals when compared to acute
and chronic sham groups. Our data has demonstrated that an
increase of APE/Ref-1 mRNA levels in the caudal region of spinal
cord strongly correlated with DNA damage after traumatic spinal
cord injury. We suggest that DNA damage can be observed both
in lesional and caudal regions of the acutely and chronically
injured groups, but DNA damage is reduced with embryonic
neural stem cell therapy.