title: Glutathione and ascorbic acid enhance recovery of Guinea pig spinal cord white matter following ischemia and acrolein exposure.
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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Department of Basic Medical Sciences, Center for Paralysis Research, School of Veterinary Medicine, Purdue University, West Lafayette, IN 47907-1244, USA. riyi@purdue.edu
authors.forename: Melissa Peasley
authors.initials: MP
authors.lastname: Logan
authors.forename: Steven
authors.initials: S
authors.lastname: Parker
authors.forename: Riyi
authors.initials: R
authors.lastname: Shi
mesh_terms: D000171:Acrolein / Q000378:metabolism / Q000494:pharmacology*; D000200:Action Potentials / Q000187:drug effects; D000818:Animals; D000975:Antioxidants / Q000378:metabolism; D001205:Ascorbic Acid / Q000378:metabolism*; D001369:Axons / Q000378:metabolism / Q000473:pathology; D005260:Female; D016166:Free Radical Scavengers / Q000378:metabolism; D005947:Glucose / Q000172:deficiency; D005978:Glutathione / Q000378:metabolism*; D006168:Guinea Pigs; D006651:Histocytochemistry; D006735:Horseradish Peroxidase / Q000378:metabolism; D007511:Ischemia / Q000378:metabolism; D010477:Perfusion; D015427:Reperfusion Injury / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D020760:Spinal Cord Ischemia / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology
chemical_list: D000975:Antioxidants; D016166:Free Radical Scavengers; D000171:Acrolein; D006735:Horseradish Peroxidase; D005978:Glutathione; D005947:Glucose; D001205:Ascorbic Acid