Polyethylene glycol immediately repairs neuronal membranes and inhibits free radical production after acute spinal cord injury
Article first published online: 2 OCT 2002
Journal of Neurochemistry
Volume 83, Issue 2, pages 471–480, October 2002
How to Cite
Luo, J., Borgens, R. and Shi, R. (2002), Polyethylene glycol immediately repairs neuronal membranes and inhibits free radical production after acute spinal cord injury. Journal of Neurochemistry, 83: 471–480. doi: 10.1046/j.1471-4159.2002.01160.x
- Issue published online: 2 OCT 2002
- Article first published online: 2 OCT 2002
- Received May 8, 2002; revised manuscript received August 2, 2002; accepted August 3, 2002.
- lipid peroxidation;
- membrane integrity;
- polyethylene glycol;
- reactive oxygen species;
- spinal cord injury
Membrane disruption and the production of reactive oxygen species (ROS) are important factors causing immediate functional loss, progressive degeneration, and death in neurons and their processes after traumatic spinal cord injury. Using an in vitro guinea pig spinal cord injury model, we have shown that polyethylene glycol (PEG), a hydrophilic polymer, can significantly accelerate and enhance the membrane resealing process to restore membrane integrity following controlled compression. As a result of PEG treatment, injury-induced ROS elevation and lipid peroxidation (LPO) levels were significantly suppressed. We further show that PEG is not an effective free radical scavenger nor does it have the ability to suppress xanthine oxidase, a key enzyme in generating superoxide. These observations suggest that it is the PEG-mediated membrane repair that leads to ROS and LPO inhibition. Furthermore, our data also imply an important causal effect of membrane disruption in generating ROS in spinal cord injury, suggesting membrane repair to be an effective target in reducing ROS genesis.