Plasma and tissue vitamin E depletion in sheep with burn and smoke inhalation injury Katsumi Shimoda a, *, Hiroaki Nakazawa a , Maret G. Traber b , Daniel L. Traber c , Motohiro Nozaki a a Department of Plastic and Reconstructive Surgery, Tokyo Women’s Medical University, Kawadacho 8-1, Shinjuku-ku, Tokyo 162-0054, Japan b Linus Pauling Institute, Oregon State University, USA c Department of Anesthesiology, University of Texas Medical Branch, TX, USA 1. Introduction Oxidative stress occurs when the level of reactive oxygen intermediates (ROIs) exceeds the antioxidant defences of the host. ROIs are produced in great quantities as a result of the respiratory burst of neutrophils, other phagocytes and endothelial cells during the inflammatory process. The pathogenesis of some effects of burn and smoke inhalation, such as acute respiratory distress syndrome (ARDS), appears to involve alterations in oxidant–antioxidant balance. Major endogenous antioxidants include a- and g-tocopherol; a- tocopherol scavenges free radicals that propagate the lipid peroxidation chain reaction, and g-tocopherol scavenges reactive nitrogen species as well. Large amounts of superoxide anions are known to be present in burn and smoke and are inactivated within a few minutes in vivo. Several studies on burn and smoke inhalation injury demonstrated that lipid peroxides appear in the systemic circulation within minutes after injury and peak a second time at 24 h [2]. Peroxynitrite is a potent oxidant produced by the reaction of nitrous oxide with superoxide anions, and is produced in burn and smoke models of injury [3]. This study aims to provide data on tissue and plasma a- and g-tocopherol levels after burn and smoke inhalation. burns 34 (2008) 1137–1141 article info Article history: Accepted 21 January 2008 Keywords: Burn Inhalation injury Sheep Vitamin E abstract Oxidants are involved in the pathogenesis of many disorders caused by burn and smoke inhalation; a- and g-tocopherols are major tissue antioxidants, and their depletion should reflect oxidant injury. To determine whether plasma and tissue vitamin E levels would thus be depleted in severe burn, prepared sheep were randomly divided into the following groups: non-injured, burn- and smoke-exposed, burned only and smoke-exposed only. All were resuscitated with Ringer’s lactate solution, mechanically ventilated and sacrificed at various time intervals. Immediately following injury plasma, lung, trachea, heart and liver tocopherols/lipids were measured and found to be significantly depleted except in the heart. Reduction of tissue g-tocopherol appeared earlier than reduction of a-tocopherol. Thus animals receiving combined burn and inhalation injury underwent marked oxidative stress, suggesting that vitamin E might be depleted also in humans with burn and smoke inhalation injury, and that appropriate supplementation should be evaluated. # 2008 Elsevier Ltd and ISBI. All rights reserved. * Corresponding author. Tel.: +81 3 3353 8111. E-mail address: kshimo420@ybb.ne.jp (K. Shimoda). available at www.sciencedirect.com journal homepage: www.elsevier.com/locate/burns 0305-4179/$34.00 # 2008 Elsevier Ltd and ISBI. All rights reserved. doi:10.1016/j.burns.2008.01.015