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1 Menssana Research, Inc., Fort Lee, NJ, 2 Dept of Medicine, New York Medical College Valhalla, New York, NY, and 3 Dept of Medicine, Saint Vincents Catholic Medical Centers of New York, Staten Island Region, NY, USA
CORRESPONDENCE: M. Phillips, Menssana Research, Inc., 1 Horizon Road Suite 1415, Fort Lee, NJ , 07024, USA. Fax: 1 2018867004. E-mail: menssana@bellatlantic.net
Keywords: breath, oxidative stress, oxygen breathing, volatile organic compounds
Received: June 21, 2002
Accepted August 14, 2002
Supplemental oxygen is often administered to induce hyperoxia in nonhypoxic patients for indications such as chest pain, despite lack of evidence of clinical benefit. Induced hyperoxia is potentially toxic, since it may increase oxidative stress and peroxidative damage to deoxyribonucleic acid, lipids and proteins.
The aim of this study was to establish whether supplemental oxygen induces oxidative stress in nonhypoxic subjects.
Breath markers of oxidative stress were measured in 31 healthy subjects before and after breathing 28% oxygen at 2.0 L·min–1 via nasal prongs for 30 min while resting. The criterion standard of oxidative stress was the breath methylated alkane contour (BMAC), a three-dimensional plot of the alveolar gradients of C4–C20 alkanes and monomethylated alkanes produced by lipid peroxidation. Volatile organic compounds (VOCs) in breath were assayed by gas chromatography and mass spectroscopy, and the BMACs before and after oxygenation were compared.
Following oxygenation, there was a significant increase in mean volume under the curve of the BMAC and in alveolar gradients of three VOCs: 3-methyltridecane, 3-methylundecane and 5-methylnonane.
Breath markers of oxidative stress were significantly increased in normal volunteers breathing supplemental oxygen for 30 min.
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