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Oxidative stress in obstructive sleep apnea: Need for continuous monitoring
Free Radical Biology & Medicine 42 (2007) 895 www.elsevier.com/locate/freeradbiomed
Letter to the Editor Oxidative stress in obstructive sleep apnea: Need for continuous monitoring
nisms should help provide insights into the pathogenesis of obstructive sleep apnea-associated complications.
We were delighted to read the Letter to the Editor submitted to Free Radical Biology & Medicine by Lloret et al. entitled “Obstructive sleep apnoea: Arterial oxygen desaturation coincides with increases in systemic oxidative stress markers measured with continuous monitoring” [1] in response to our review article “Oxidative stress and oxidant signaling in obstructive sleep apnea and associated cardiovascular diseases” [2]. A review of the existing literature shows that some recent experiments indicated the occurrence of oxidative stress, while others did not [2]. These controversies might be due to experimental protocols used by studies in which samples were taken before and/or after, but not during, sleep. Thus, experiments presented by Lloret et al. [1] represent an important strategy by taking samples during sleep, more specifically when patients are subjected to apnea-associated hypoxemia. With their approach in which blood samples were taken concomitant with sleep apnea and associated desaturation, authors report quite interesting observations that indicators of oxidative stress were visible at the time of desaturation, but cease immediately after it [1]. More intriguingly, such induction of oxidative stress was only seen during the first hour after sleep [1]. While further studies are needed to confirm these interesting observations, these experiments potentially suggest that hypoxia might trigger the production of reactive oxygen species, consistent with suggestions by Schumacker and coworkers in their experimental models [3]. Such responses, however, seem to be followed by activation of adaptive mechanisms, which turn off the ability to produce reactive oxygen species after the first hour of sleep. The cessation of oxidative stress production immediately after desaturation as well as adaptation after the first hour of sleep to eliminate the hypoxemia-induced oxidant production might explain the inability of some of the studies to observe oxidative stress in obstructive sleep apnea patients. In summary, we believe that Lloret et al. [1] have provided important preliminary results which suggest the need for continuously monitoring oxidative stress parameters during sleep in order to accurately assess the production of oxidants in obstructive sleep apnea patients. These experiments also suggested that biological systems may possess mechanisms to turn on and off the production of reactive oxygen species in response to intermittent hypoxia. Understanding such mecha-
Acknowledgments
0891-5849/$ - see front matter © 2007 Elsevier Inc. All rights reserved. doi:10.1016/j.freeradbiomed.2006.12.016
This work was supported in part by National Institutes of Health Grants HL67340 (to Y.J.S.), HL72844 (to Y.J.S.), and HL73929 (to R.M.D.). The information in this manuscript is the opinion of the authors and does not reflect the views of the Uniformed Services University of the Health Sciences, the US Department of Defense, or the US Federal Government.
References [1] Lloret, A.; Buj, J.; Badia, M. C.; Sastre, J.; Morera, J.; Vina, J. Obstructive sleep apnoea: Arterial oxygen desaturation coincides with increases in systemic oxidative stress markers measured with continuous monitoring. Free Radic. Biol. Med. 42:893–894; 2007. [2] Suzuki, Y. J.; Jain, V.; Park, A. M.; Day, R. M. Oxidative stress and oxidant signaling in obstructive sleep apnea and associated cardiovascular diseases. Free Radic. Biol. Med. 40:1683–1692; 2006. [3] Guzy, R. D.; Schumacker, P. T. Oxygen sensing by mitochondria at complex III: the paradox of increased reactive oxygen species during hypoxia. Exp. Physiol. 91:807–819; 2006.
Yuichiro J. Suzuki* Ah-Mee Park Department of Pharmacology, Georgetown University Medical Center, Room NW403, Medical-Dental Building, 3900 Reservoir Road NW, Washington, DC 20057, USA E-mail address: [email protected]. ⁎Corresponding author. Fax: +1 202 687 2585. Vivek Jain Division of Pulmonary and Critical Care Medicine, Department of Medicine, George Washington University Medical Center, Washington, DC 20037, USA Regina M. Day Department of Pharmacology, Uniformed Services University of the Health Sciences, Bethesda, MD 20814, USA 12 November 2006
Letter to the Editor Oxidative stress in obstructive sleep apnea: Need for continuous monitoring
nisms should help provide insights into the pathogenesis of obstructive sleep apnea-associated complications.
We were delighted to read the Letter to the Editor submitted to Free Radical Biology & Medicine by Lloret et al. entitled “Obstructive sleep apnoea: Arterial oxygen desaturation coincides with increases in systemic oxidative stress markers measured with continuous monitoring” [1] in response to our review article “Oxidative stress and oxidant signaling in obstructive sleep apnea and associated cardiovascular diseases” [2]. A review of the existing literature shows that some recent experiments indicated the occurrence of oxidative stress, while others did not [2]. These controversies might be due to experimental protocols used by studies in which samples were taken before and/or after, but not during, sleep. Thus, experiments presented by Lloret et al. [1] represent an important strategy by taking samples during sleep, more specifically when patients are subjected to apnea-associated hypoxemia. With their approach in which blood samples were taken concomitant with sleep apnea and associated desaturation, authors report quite interesting observations that indicators of oxidative stress were visible at the time of desaturation, but cease immediately after it [1]. More intriguingly, such induction of oxidative stress was only seen during the first hour after sleep [1]. While further studies are needed to confirm these interesting observations, these experiments potentially suggest that hypoxia might trigger the production of reactive oxygen species, consistent with suggestions by Schumacker and coworkers in their experimental models [3]. Such responses, however, seem to be followed by activation of adaptive mechanisms, which turn off the ability to produce reactive oxygen species after the first hour of sleep. The cessation of oxidative stress production immediately after desaturation as well as adaptation after the first hour of sleep to eliminate the hypoxemia-induced oxidant production might explain the inability of some of the studies to observe oxidative stress in obstructive sleep apnea patients. In summary, we believe that Lloret et al. [1] have provided important preliminary results which suggest the need for continuously monitoring oxidative stress parameters during sleep in order to accurately assess the production of oxidants in obstructive sleep apnea patients. These experiments also suggested that biological systems may possess mechanisms to turn on and off the production of reactive oxygen species in response to intermittent hypoxia. Understanding such mecha-
Acknowledgments
0891-5849/$ - see front matter © 2007 Elsevier Inc. All rights reserved. doi:10.1016/j.freeradbiomed.2006.12.016
This work was supported in part by National Institutes of Health Grants HL67340 (to Y.J.S.), HL72844 (to Y.J.S.), and HL73929 (to R.M.D.). The information in this manuscript is the opinion of the authors and does not reflect the views of the Uniformed Services University of the Health Sciences, the US Department of Defense, or the US Federal Government.
References [1] Lloret, A.; Buj, J.; Badia, M. C.; Sastre, J.; Morera, J.; Vina, J. Obstructive sleep apnoea: Arterial oxygen desaturation coincides with increases in systemic oxidative stress markers measured with continuous monitoring. Free Radic. Biol. Med. 42:893–894; 2007. [2] Suzuki, Y. J.; Jain, V.; Park, A. M.; Day, R. M. Oxidative stress and oxidant signaling in obstructive sleep apnea and associated cardiovascular diseases. Free Radic. Biol. Med. 40:1683–1692; 2006. [3] Guzy, R. D.; Schumacker, P. T. Oxygen sensing by mitochondria at complex III: the paradox of increased reactive oxygen species during hypoxia. Exp. Physiol. 91:807–819; 2006.
Yuichiro J. Suzuki* Ah-Mee Park Department of Pharmacology, Georgetown University Medical Center, Room NW403, Medical-Dental Building, 3900 Reservoir Road NW, Washington, DC 20057, USA E-mail address: [email protected]. ⁎Corresponding author. Fax: +1 202 687 2585. Vivek Jain Division of Pulmonary and Critical Care Medicine, Department of Medicine, George Washington University Medical Center, Washington, DC 20037, USA Regina M. Day Department of Pharmacology, Uniformed Services University of the Health Sciences, Bethesda, MD 20814, USA 12 November 2006