Original article Oxygen toxicity: simultaneous measure of pentane and malondialdehyde in humans exposed to hyperoxia M.N. Loiseaux-Meunier 1 *, M. Bedu 2 , C. Gentou 1 , D. Pepin 3 , J. Coudert 2 , D. Caillaud 4 1 Laboratoire de Biochimie Médicale et Immunochimie, Hôpital Gabriel-Montpied, 30, place Henri-Dunant, 63000 Clermont-Ferrand, France; 2 Laboratoire d’Explorations Fonctionnelles Respiratoires et Sportives, Hôpital Gabriel- Montpied, 30, place Henri-Dunant, 63000 Clermont-Ferrand, France; 3 Laboratoire d’Hydrologie et d’Hygiène, Institut Louise Blanquet, Faculté de Médecine et de Pharmacie, 28, place Henri-Dunant, 63000 Clermont-Ferrand, France; 4 Service de Pneumologie, Hôpital Gabriel-Montpied, 30, place Henri-Dunant, 63000 Clermont-Ferrand, France (Received 24 October 2000; accepted 3 December 2000) Summary – In order to estimate cell damage caused by free radicals during oxygenotherapy, we investigated the time course of two markers of lipoperoxidation: pentane in breath and malondialde- hyde (MDA) in blood during brief normobaric hyperoxia. Nine healthy subjects inhaled hydrocarbon- free air (HCFA) for 30 minutes, hydrocarbon-free 100% O 2 (HCFO 2 ) for 125 minutes and then HCFA for 70 minutes. After 15 minutes of washout with HCFA, ambient pentane was eliminated. After HCFO 2 , at T175 ver- sus T30 (i.e., 145 min from the start of 100% HCFO 2 ), pentane production increased (P < 0.05). MDA rose significantly at T155 min (i.e., 125 min from the start of HCFO 2 ), versus T30 (P < 0.01). These results suggest that acute hyperoxia causes a moderate increase in lipid peroxidation in healthy subjects. The increase of pentane and MDA confirms that acute hyperoxia induces lipid peroxidation in healthy subjects. © 2001 Éditions scientifiques et médicales Elsevier SAS malondialdehyde / normobaric hyperoxia / pentane Oxygen delivery at higher than ambient concentra- tion will stay in frequent clinical use until 100% oxy- gen can be used in the care of critically ill patients. The benefits of oxygen therapy have been known for many years; however, its potential toxicity has only been recognized in the last two decades. The toxic FIO 2 threshold (length of exposure and level) is still debated and research is continuing to prevent, diag- nose and treat this disorder. Biochemical theory to explain oxygen toxicity is generally attributed to the increase of the formation of oxygen-free radicals. In air, only 1 to 2% of oxy- gen undergoes univalent reduction, producing the superoxide radical (O 2 – ) and derivatives. However, at high oxygen exposure, oxygen-derived radicals are generated at a rate exceeding the body’s antioxidant capacity. Uncontrolled free radicals react with poly- unsaturated fatty acids (PUFA) of cell membranes and initiate lipid peroxidation. Lipoperoxidation due to hyperoxia can be evalu- ated with various biological markers: F2-isoprostane in alveolar macrophages [1], malondialdehyde (MDA) in blood or in tissues [2-5], dienes conjugate in erythrocytes [6], hydroperoxides in blood [7] and alkanes (ethane, pentane) in breath air [8-10]. Malondialdehyde, a major compound of lipoper- oxidation, is most generally used in clinical biology *Correspondence and reprints. E-mail address: mnmeunier@chu-clermontferrand.fr (M.N. Loiseaux- Meunier). Biomed Pharmacother 2001 ; 55 : 163-9 © 2001 Éditions scientifiques et médicales Elsevier SAS. All rights reserved S0753332201000427/FLA