title: Burn and smoke inhalation injury in sheep depletes vitamin E: kinetic studies using deuterated tocopherols.
abstract: To test the hypothesis that burn and smoke injury will deplete tissue alpha-tocopherol and cause its faster plasma disappearance, deuterium-labeled vitamin E was administered to sheep exposed to both surface skin burn and smoke insufflation, which cause injuries similar to those of human victims of fire accidents. Two different protocols were used: (1) deuterated vitamin E was administered orally with food at time 0 (just before injury) or (2) the labeled vitamin E was administered orally with food the day before injury. The animals, which had been operatively prepared seven days before, were anesthetized and then received both 40% body surface area third-degree burn and 48 breaths of cotton smoke or sham injuries. All were resuscitated with Ringer's lactate solution (4 ml/kg/% BSA burn/24 h) and mechanically ventilated. Blood samples were collected at various times after vitamin E dosing. In both studies the depletion of plasma alpha-tocopherol was faster in the injured sheep. The sheep given deuterated vitamin E 24 h before injury had similar maximum alpha-tocopherol concentrations at similar times. The exponential rates of alpha-tocopherol disappearance were 1.5 times greater and half-lives were 12 h shorter (p < 0.05) in the injured sheep. In separate studies, various tissues were obtained from sheep that were sacrificed from 4 to 48 h after injury. The liver alpha-tocopherol concentrations in sheep killed at various times after injury seem to show a linear decrease at a rate of 0.1 nmol alpha-tocopherol/g liver per hour, suggesting that the liver is supplying alpha-tocopherol to maintain the plasma and lung alpha-tocopherol concentrations, but that this injury is so severe the liver is unable to maintain lung alpha-tocopherol concentrations. These findings suggest that alpha-tocopherol should be administered to burn patients to prevent vitamin E depletion and to protect against oxidative stress from burn injury.
authors: Linus Pauling Institute, Oregon State University, Corvallis, OR 97331, USA. maret.traber@oregonstate.edu
authors: M G
authors: MG
authors: Traber
authors: K
authors: K
authors: Shimoda
authors: K
authors: K
authors: Murakami
authors: S W
authors: SW
authors: Leonard
authors: P
authors: P
authors: Enkhbaatar
authors: L D
authors: LD
authors: Traber
authors: D L
authors: DL
authors: Traber
mesh_terms: D000818:Animals; D002056:Burns / Q000150:complications*; D003903:Deuterium; D004195:Disease Models, Animal; D007700:Kinetics; D012756:Sheep; D012906:Smoke / Q000009:adverse effects*; D012907:Smoking / Q000009:adverse effects*; D013997:Time Factors; D014810:Vitamin E / Q000378:metabolism*; D014811:Vitamin E Deficiency / Q000209:etiology*; D014851:Wakefulness
chemical_list: D012906:Smoke; D014810:Vitamin E; D003903:Deuterium