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Review
. 2006 May 15;40(10):1683-92.
doi: 10.1016/j.freeradbiomed.2006.01.008. Epub 2006 Feb 2.

Oxidative stress and oxidant signaling in obstructive sleep apnea and associated cardiovascular diseases

Yuichiro J Suzuki  1 , Vivek Jain, Ah-Mee Park, Regina M Day
Affiliations
Review

Oxidative stress and oxidant signaling in obstructive sleep apnea and associated cardiovascular diseases

Yuichiro J Suzuki et al. Free Radic Biol Med. .

Abstract

Obstructive sleep apnea (OSA) has emerged as a major public health problem and increasing evidence indicates that untreated OSA can lead to the development of various cardiovascular disorders. One important mechanism by which OSA may promote cardiovascular diseases is intermittent hypoxia, in which patients are subjected to repeated episodes of brief oxygen desaturation in the blood, followed by reoxygenation. Such cycles of hypoxia/reoxygenation may result in the generation of reactive oxygen species. Some studies have demonstrated the presence of oxidative stress in OSA patients as well as in animals subjected to intermittent hypoxia. Further, modulations of nitric oxide and biothiol status might also play important roles in the pathogenesis of OSA-associated diseases. Reactive oxygen species and redox events are also involved in the regulation of signal transduction for oxygen-sensing mechanisms. This review summarizes currently available information on the evidence for and against the occurrence of oxidative stress in OSA and the role of reactive oxygen species in cardiovascular changes associated with OSA.

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Figures

Fig. 1
Fig. 1
Effects of intermittent hypoxia on ischemia/reperfusion-induced myocardial lipid peroxidation and cardiac muscle cell apoptosis. C57BL/6 mice were subjected to intermittent hypoxia (2 min cycles of 6 and 21% O2) for 8 h/day for 2 weeks (2w). After intermittent hypoxia, isolated hearts were subjected to 30 min ischemia followed by reperfusion. (A) Hearts were homogenized and the levels of malondialdehyde (MDA) were monitored as an indication for lipid peroxidation. (B) Hearts were stained to assess TUNEL-positive cells as an indication for apoptosis. Values represent means ± SE. (*) denotes the values that are significantly different from control (con) at P b 0.05.
Fig. 2
Fig. 2
Schematics of the roles of ROS in OSA-mediated cardiac hypertrophy.
See this image and copyright information in PMC

Comment in

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