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Am. J. Respir. Crit. Care Med., Volume 162, Number 2, August 2000, 369-373

Exhaled Ethane, a Marker of Lipid Peroxidation, Is Elevated in Chronic Obstructive Pulmonary Disease

PAOLO PAREDI, SERGEI A. KHARITONOV, DAVID LEAK, SIMON WARD, DAVID CRAMER, and PETER J. BARNES

Department of Thoracic Medicine, Imperial College School of Medicine at the National Heart and Lung Institute; Department of Biochemistry, Imperial College of Science, Technology and Medicine; and Lung Function Unit, Royal Brompton Hospital, London, United Kingdom

Ethane is a product of lipid peroxidation and can be measured in the exhaled air as an index of oxidative stress. Oxidant/antioxidant imbalance is important in the pathogenesis of chronic obstructive pulmonary disease (COPD). Therefore, we measured exhaled ethane in 22 patients with COPD (mean age ± SEM, 59 ± 8 yr; 19 male) and compared it with other noninvasive markers of oxidative stress and inflammation such as carbon monoxide (CO), measured electrochemically, and nitric oxide (NO), measured by chemiluminescence. Exhaled ethane was collected during a flow and pressure-controlled exhalation into a reservoir, discarding dead space air contaminated with ambient air. A sample of the collected expired air was analyzed by chromatography. Compared with normal subjects (n = 14; eight men; age, 33 ± 2.8 yr), patients with COPD not on steroid treatment (n = 12; FEV1, 58 ± 6%) had elevated levels of exhaled ethane (2.77 ± 0.25 and 0.88 ± 0.09 ppb, respectively, p < 0.05), CO (5.96 ± 0.50 and 2.8 ± 0.25 ppm, p < 0.05) and NO (11.86 ± 0.53 and 6.77 ± 0.50 ppb, p < 0.05) levels. Ethane was correlated to FEV1 (r = -0.67, p < 0.05). Patients receiving steroid treatment (n = 10; FEV1, 56 ± 2%) had lower levels of ethane (0.48 ± 0.05 ppb) than did steroid-treated patients, whereas CO (5.99 ± 0.63 ppm) and NO (9.11 ± 0.53 ppb) levels were similar in the two treatment groups. Exhaled ethane is elevated, correlates with FEV1, and is significantly lower in patients treated with steroids, so it may be complementary to the use of NO and CO in assessing and monitoring oxidative stress in COPD.




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