SHORT COMMUNICATION Urinary F 2 -isoprostane metabolite levels in children with sleep-disordered breathing Hawley E. Montgomery-Downs & Jyoti Krishna & L. Jackson Roberts II & David Gozal # Springer-Verlag 2006 Abstract Oxidant stress-related mechanisms have been proposed as a major contributor to the increased prevalence of cardiovascular morbidity in adult patients with sleep- disordered breathing. Isoprostanes provide a reliable bio- marker of oxidant injury in vivo. The purpose of the present study was to examine the hypothesis that oxidant stress, as evidenced by increased levels of F 2 -isoprostane metabolites (IsoP-m) in urine, is present in children with a spectrum of sleep-disordered breathing. Assays were performed on urinary samples obtained from each of 47 pediatric patients immediately upon awakening after standard overnight polysomnography. Of the subjects, 15% had mild, 9% had moderate, and 6% had severe sleep-disordered breathing. After controlling for correlations between BMI and IsoP-m and SpO2 values, IsoP-m values were unrelated to any polysomnographic measures. The absence of increased levels of urinary F 2 -isoprostane metabolites in children with sleep-disordered breathing suggests that oxidative stress is not a significant feature of pediatric sleep- disordered breathing. Keywords Oxidant stress . Sleep-disordered breathing . Pediatric . Isoprostane Introduction Oxidant stress-related mechanisms were proposed as a major contributor to cardiovascular morbidity in adult patients with sleep-disordered breathing (SDB) [1, 2], and there is evidence of their improvement after continuous positive airway pressure (CPAP) treatment [3–6]. The cumulative findings suggest that intermittent hyp- oxia associated with SDB may activate a cascade of oxidant stress reactions which targets lipid-related compounds, and thereby favoring the onset and acceleration of atherogene- sis. Furthermore, episodic hypoxia in a rodent model of SDB [7] leads to increased oxidant stress and is mechanis- tically associated with neurobehavioral deficits [8–10]. Studies have also questioned the relationship between oxidant stress and SDB in adults. Wali et al. found no oxidative stress differences between normal controls and those with obstructive sleep apnea (OSA) with no changes after treatment with CPAP [11]. Although it was a split- night study, Svatikova et al. found no change in markers of oxidative stress and lipid peroxidation compared to controls [12]. F 2 -isoprostanes are specific products of lipid peroxida- tion and their metabolites were validated for the assessment of oxidative stress in vivo [13, 14], specifically within the pediatric population [15]. F 2 -isoprostanes are a family of Sleep Breath DOI 10.1007/s11325-006-0079-5 H. E. Montgomery-Downs Department of Psychology, West Virginia University, 53 Campus Drive, Morgantown, WV 26506-6040, USA J. Krishna Kosair Children’ s Hospital Research Institute, and Division of Pediatric Sleep Medicine, Department of Pediatrics, University of Louisville, 571 South Floyd Street, Louisville, KY 40202, USA L. J. Roberts II Departments of Pharmacology and Medicine, Vanderbilt University, 2222 Pierce Ave, Nashville, TN 37232, USA D. Gozal (*) Kosair Children’ s Hospital Research Institute, University of Louisville School of Medicine, 570 South Preston Street, Suite 204, Louisville, KY 40202, USA e-mail: david.gozal@louisville.edu