“…Therefore, high oxygen supplementation coupled with low SOD activity add to oxidative stress, and this may be evidenced by an increase in the by-products of lipid peroxidation (lipid peroxides, malondialdehyde, HNE, alkanes such as ethane and pentane, and isoprostanes) and/or of protein oxidation (carbonyl compounds, o-dityrosine). Newborn infants receiving O 2 supplementation have demonstrably elevated levels of markers of oxidative stress such as exhaled ethane and pentane (Nycyk et al, 1998;Pitkanen et al, 1990), serum HNE (Ogihara et al, 1999), F 2a -isoprostanes in tracheal aspirate or in plasma (Ahola et al, 2004), protein-carbonyl in bronchoalveolar fluid (Gladstone & Levine et al, 1994) or o-dityrosine in urine (Kelly & Lubec, 1995;Lubec et al, 1997). It has been suggested that some of these markers may be higher in the first few days of life in preterm infants who will develop BPD as compared to those who will not (Gladstone & Levine et al, 1994;Hodgman et al, 1969).…”