title: Effect of vitamin E supplementation on hypoxia-induced oxidative damage in male albino rats.
abstract: BACKGROUND
  There is growing evidence that free radicals mediated oxidative injury due to inadequate oxygen availability is an important factor in various pathologies at high altitude. Since vitamin E is known to protect the cells from oxidative damage due to its potent antioxidant properties, the present study was carried out to explore the effect of vitamin E supplementation on various hematological and biochemical parameters in hypoxia-induced oxidative stress in albino rats.
  
  
  METHODS
  The experiments were conducted on male albino rats by intermittently exposing them to a simulated altitude of 7,576 m (25,000 ft), daily for 6 h for 15 d at 32 +/- 2 degrees C. The control group was fed vehicle only (1% Tween 80) and the experimental group was given vitamin E (40 mg per rat x d(-1)) orally, 5 d prior to and during the period of hypoxic exposure. The variables studied include: hemoglobin, hematocrit, RBC deformability index, alpha-tocopherol level, malondialdehyde (MDA), reduced glutathione (GSH), oxidized glutathione (GSSG), lactate dehydrogenase (LDH) and protein level in blood/plasma and various tissues.
  
  
  RESULTS
  Significant increase in hematocrit and hemoglobin and decrease in RBC deformability index was observed on exposure to hypoxia while vitamin E supplementation maintained them at the normal level. Hypoxia led to the decrease in plasma vitamin E and blood glutathione (GSH) level and two-fold increase in the plasma malondialdehyde (MDA) level. Vitamin E supplementation, on the other hand, resulted in less of an increase in MDA and increased the GSH concentration significantly. LDH activity, which was elevated on exposure to hypoxia, was arrested on vitamin E supplementation.
  
  
  CONCLUSIONS
  The results indicate that vitamin E supplementation results in preventing oxidative damage due to high altitude stress.
authors.affiliation: Defence Institute of Physiology and Allied Sciences, Timarpur, Ministry of Defence, Delhi, India. defphysiol@satyam.net.in
authors.forename: G
authors.initials: G
authors.lastname: Ilavazhagan
authors.forename: A
authors.initials: A
authors.lastname: Bansal
authors.forename: D
authors.initials: D
authors.lastname: Prasad
authors.forename: P
authors.initials: P
authors.lastname: Thomas
authors.forename: S K
authors.initials: SK
authors.lastname: Sharma
authors.forename: A K
authors.initials: AK
authors.lastname: Kain
authors.forename: D
authors.initials: D
authors.lastname: Kumar
authors.forename: W
authors.initials: W
authors.lastname: Selvamurthy
mesh_terms: D000531:Altitude; D000818:Animals; D000975:Antioxidants / Q000494:pharmacology*; D019587:Dietary Supplements; D005978:Glutathione / Q000097:blood; D000860:Hypoxia / Q000503:physiopathology*; D007770:L-Lactate Dehydrogenase / Q000097:blood; D008297:Male; D008315:Malondialdehyde / Q000097:blood; D018384:Oxidative Stress / Q000187:drug effects*; D051381:Rats; D017207:Rats, Sprague-Dawley; D014810:Vitamin E / Q000494:pharmacology*
chemical_list: D000975:Antioxidants; D014810:Vitamin E; D008315:Malondialdehyde; D007770:L-Lactate Dehydrogenase; D005978:Glutathione