title: Lipid peroxidation does not appear to be a factor in late radiation injury of the cervical spinal cord of rats.
abstract: OBJECTIVE
  We tested the role of lipid peroxidation in the demyelination and white matter necrosis associated with radiation injury of the central nervous system.
  
  
  METHODS
  We irradiated the cervical spinal cords of female F344 rats (23 Gy) and assayed for the accumulation of the peroxidation byproducts malondialdehyde and hydroxyeicosatetraenoic acids, and for the consumption of the endogenous free radical scavengers vitamins E and C. We further tested the role of lipid peroxidation in radiation injury of the central nervous system by determining the sensitivity of the cervical spinal cord to radiation in rats on diets containing deficient, normal, and supplemental levels of the antioxidant vitamin E. Rats were placed on these diets at 4 weeks of age and irradiated (18.5-21.5 Gy) 16 weeks later.
  
  
  RESULTS
  During the 5 months between irradiation and the onset of paralysis, no accumulation of peroxidation byproducts or consumption of endogenous scavengers was seen in the cervical spinal cords of the irradiated rats. The cervical spinal cords of some of the rats placed on the diets with deficient, normal, and supplemental levels of vitamin E were analyzed at the time of irradiation and contained 197 +/- 57, 501 +/- 19, and 717 +/- 35 pmol vitamin E/mg protein, respectively. Despite the statistical differences in these levels, the radiation sensitivity of the cervical spinal cord (ED50 for white matter necrosis) in rats receiving the three diets was not different (20.4, 20.7, and 20.6 Gy).
  
  
  CONCLUSIONS
  These data do not support a role for free radical-induced lipid peroxidation in the white matter damage seen in radiation injury of the central nervous system.
authors.affiliation: Department of Neurological Surgery, School of Medicine, University of California, San Francisco.
authors.forename: P H
authors.initials: PH
authors.lastname: Gutin
authors.forename: K J
authors.initials: KJ
authors.lastname: Levin
authors.forename: M W
authors.initials: MW
authors.lastname: McDermott
authors.forename: N
authors.initials: N
authors.lastname: Hooper
authors.forename: M T
authors.initials: MT
authors.lastname: Smith
authors.forename: J R
authors.initials: JR
authors.lastname: Cashman
authors.forename: P H
authors.initials: PH
authors.lastname: Chan
authors.forename: G Y
authors.initials: GY
authors.lastname: Ross
authors.forename: T L
authors.initials: TL
authors.lastname: Phillips
authors.forename: V A
authors.initials: VA
authors.lastname: Levin
mesh_terms: D000818:Animals; D001205:Ascorbic Acid / Q000378:metabolism; D005260:Female; D016166:Free Radical Scavengers; D006893:Hydroxyeicosatetraenoic Acids / Q000096:biosynthesis; D015227:Lipid Peroxidation / Q000502:physiology*; D008315:Malondialdehyde / Q000378:metabolism; D011833:Radiation Injuries, Experimental / Q000503:physiopathology*; D051381:Rats; D011916:Rats, Inbred F344; D013116:Spinal Cord / Q000378:metabolism / Q000528:radiation effects*; D013997:Time Factors; D014810:Vitamin E / Q000378:metabolism
chemical_list: D016166:Free Radical Scavengers; D006893:Hydroxyeicosatetraenoic Acids; D014810:Vitamin E; D008315:Malondialdehyde; D001205:Ascorbic Acid