title: Effects of vitamin E on oxidative stress and membrane fluidity in brain of streptozotocin-induced diabetic rats.
abstract: BACKGROUND
  Diabetics and experimental animal models exhibit high oxidative stress due to persistent and chronic hyperglycemia, thereby deplete the activity of the antioxidative defense system and thereby promote the generation of free radicals. The current study examined the effects of vitamin E on oxidative stress and membrane fluidity in the brain of diabetes-induced rats.
  
  
  METHODS
  Sprague-Dawley male rats were randomly assigned to normal and streptozotocin (STZ)-induced diabetic groups. The diabetic groups were fed a vitamin E-free diet, 40 mg vitamin E/kg diet, or 400 mg vitamin E/kg diet. Diabetes was induced with STZ after 3 weeks of the experimental diet, then the rats were sacrificed 9 days later to determine the oxidative stress and cell membrane fluidity in the brain.
  
  
  RESULTS
  Dietary vitamin E strengthened the antioxidative defense system with an increased activity of the antioxidant enzymes, such as superoxide dismutase (SOD) and glutathione peroxidase (GSH-px) and increased vitamin E content, in the brain of the diabetes-induced experimental rats. Accordingly, vitamin E was found to reduce the accumulation of reactive oxygen species (ROS), such as superoxide radical decrease the generation of oxidative damage substances, such as the carbonyl value, increase the membrane fluidity lowered by oxidative damage, and significantly improve the lipid composition.
  
  
  CONCLUSIONS
  Vitamin E was found to be excellent for strengthening the antioxidative defense system, reducing the generation of ROS and damaging oxidative substances, and maintaining membrane fluidity in the brain of diabetes-induced rats.
authors.affiliation: Department of Food Science and Nutrition, Catholic University of Daegu, Gyeongsan-si, Gyeongbuk 712-702, South Korea.
authors.forename: Jung-Hee
authors.initials: JH
authors.lastname: Hong
authors.forename: Mi-Ji
authors.initials: MJ
authors.lastname: Kim
authors.forename: Mo-Ra
authors.initials: MR
authors.lastname: Park
authors.forename: Oh-Gye
authors.initials: OG
authors.lastname: Kwag
authors.forename: In-Seon
authors.initials: IS
authors.lastname: Lee
authors.forename: Boo Hyeong
authors.initials: BH
authors.lastname: Byun
authors.forename: Soo-Chun
authors.initials: SC
authors.lastname: Lee
authors.forename: Kyung-Bok
authors.initials: KB
authors.lastname: Lee
authors.forename: Soon-Jae
authors.initials: SJ
authors.lastname: Rhee
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000008:administration & dosage / Q000494:pharmacology*; D001921:Brain / Q000187:drug effects* / Q000378:metabolism; D002784:Cholesterol / Q000378:metabolism; D003921:Diabetes Mellitus, Experimental / Q000139:chemically induced / Q000378:metabolism* / Q000473:pathology*; D008297:Male; D008560:Membrane Fluidity / Q000187:drug effects*; D018384:Oxidative Stress / Q000187:drug effects* / Q000502:physiology; D010743:Phospholipids / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D017382:Reactive Oxygen Species / Q000378:metabolism; D013311:Streptozocin / Q000494:pharmacology; D014280:Triglycerides / Q000378:metabolism; D014810:Vitamin E / Q000008:administration & dosage / Q000494:pharmacology*
chemical_list: D000975:Antioxidants; D010743:Phospholipids; D017382:Reactive Oxygen Species; D014280:Triglycerides; D014810:Vitamin E; D013311:Streptozocin; D002784:Cholesterol