title: Effects of EPC-K1 on lipid peroxidation in experimental spinal cord injury.
abstract: METHODS
  A study in which levels of lipid peroxidation were measured, the thiobarbituric acid-reactive substances were estimated in an experimental rat model, and the recovery was assessed.
  
  
  OBJECTIVE
  To ascertain the occurrence of thiobarbituric acid-reactive substances in the damaged spinal cord, and to investigate the effectiveness of a hydroxyl radical scavenger EPC-K1, a phosphate diester linkage of vitamins E and C, in attenuating the severity of spinal cord injury.
  
  
  BACKGROUND
  Lipid peroxidation has been reported to play an important role in spinal cord injury. There is no report on the use of EPC-K1 to attenuate the severity of spinal cord injury in either animal or human studies.
  
  
  METHODS
  Spinal cord injury was induced by placing a 25-g weight on T12, and the animals were divided into six groups. Group 1 (sham) received only laminectomy. Group 2 (control) received spinal cord injury. Group 3 received EPC-K1 5 minutes before injury. Group 4 received it 5 minutes after injury. Group 5 received it 3 hours after injury. Group 6 received it five times, respectively: at 5 minutes, then 1, 2, 3, and 4 hours after injury. The levels of thiobarbituric acid-reactive substances were measured in the spinal cord, and the recovery was assessed.
  
  
  RESULTS
  The thiobarbituric acid-reactive substances content increased after injury, with two peaks, at 1 and 4 hours. Concentration at the 4-hour peak was lower in nitrogen mustard-induced leukocytopenia rats than in the control rats. The EPC-K1 injection reduced thiobarbituric acid-reactive substances content at 1 and 4 hours after injury in Group 3 (respectively, 34.3% and 42.7% vs. control) and only that at 4 hours in Group 6 (24.9% vs. control). Motor function recovery and histologic findings were better in these two groups than in Group 2.
  
  
  CONCLUSIONS
  Repeated injection of EPC-K1 attenuated the severity of spinal cord injury.
authors.affiliation: Department of Orthopedic Surgery, Kumamoto University School of Medicine, Japan. torufuji@kaiju.medic.kumamoto-u.ac.jp
authors.forename: T
authors.initials: T
authors.lastname: Fujimoto
authors.forename: T
authors.initials: T
authors.lastname: Nakamura
authors.forename: T
authors.initials: T
authors.lastname: Ikeda
authors.forename: Y
authors.initials: Y
authors.lastname: Taoka
authors.forename: K
authors.initials: K
authors.lastname: Takagi
mesh_terms: D000477:Alkylating Agents / Q000494:pharmacology; D000818:Animals; D001205:Ascorbic Acid / Q000031:analogs & derivatives* / Q000494:pharmacology; D016166:Free Radical Scavengers / Q000494:pharmacology*; D007958:Leukocyte Count / Q000187:drug effects; D015227:Lipid Peroxidation / Q000187:drug effects*; D008297:Male; D008466:Mechlorethamine / Q000494:pharmacology; D009043:Motor Activity / Q000187:drug effects; D051381:Rats; D017208:Rats, Wistar; D013119:Spinal Cord Injuries / Q000473:pathology / Q000503:physiopathology / Q000517:prevention & control*; D018709:Statistics, Nonparametric; D017392:Thiobarbituric Acid Reactive Substances / Q000032:analysis; D014810:Vitamin E / Q000031:analogs & derivatives* / Q000494:pharmacology
chemical_list: D000477:Alkylating Agents; D016166:Free Radical Scavengers; D017392:Thiobarbituric Acid Reactive Substances; D014810:Vitamin E; D008466:Mechlorethamine; C066638:potassium ascorbyl tocopheryl phosphate; D001205:Ascorbic Acid