Address of Corresponding Author

Pathobiology 2005;72:171-178 (DOI: 10.1159/000086786)

  Key Words

• Neurotrauma
• Oxygen glucose deprivation
• Reperfusion
• Membrane
• Antioxidants

  Abstract

Objective: We have shown that acrolein, a lipid peroxidation byproduct, can inflict significant damage in isolated spinal cord white matter following oxygen glucose deprivation (OGD). The mechanism of such acrolein-induced damage is unclear. The aim of this study was to examine whether glutathione (GSH) and ascorbic acid, two reactive oxygen species (ROS) scavengers, can alleviate functional and anatomical damage due to acrolein. Methods: We used an OGD injury model with isolated guinea pig spinal cord white matter. Sucrose gap recording was used to monitor axonal impulse conduction, and a horseradish peroxidase exclusion test was employed to determine membrane integrity. The functional and anatomical parameters were compared in three groups: acrolein, acrolein/GSH and acrolein/ascorbic acid. Results: We found that while GSH resulted in an 87% recovery of compound action potential conductance, ascorbic acid produced a 97% recovery, compared with a 69% recovery in an injured group without treatment. It is noted that GSH, and to a lesser extent ascorbic acid, preferentially enhanced functional recovery in smaller axons. Conclusion: Acrolein-induced neuronal damage is likely mediated by ROS. Furthermore, GSH and ascorbic acid are effective in suppressing acrolein and free radical-induced injury in spinal cord white matter.

Copyright © 2005 S. Karger AG, Basel

  Author Contacts

Prof. Riyi Shi, MD, PhD
Department of Basic Medical Sciences, Center for Paralysis Research
School of Veterinary Medicine, Purdue University
West Lafayette, IN 47907-1244 (USA)
Tel. +1 765 496 3018, Fax +1 765 494 7605, E-Mail riyi@purdue.edu

  Article Information

Received: September 20, 2004
Accepted: December 30, 2004
Number of Print Pages : 8
Number of Figures : 5, Number of Tables : 0, Number of References : 40