Oxidative Stress Markers among Obstructive Sleep Apnea Patients

Abstract

Obstructive sleep apnea (OSA) is a chronic respiratory disorder, which can be present in up to 50% of the population, depending on the country. OSA is characterized by recurrent episodes of partial or complete obstruction of the upper airways with consistent movement of the respiratory musculature during sleep. Apneas and hypopneas can lead to a decrease in oxygen saturation, an increase in carbon dioxide in the blood, and subsequent arousals and sleep fragmentation caused by repetitive activation of the central nervous system. As a consequence, intermittent hypoxemia and consequent reoxygenation result in the production of reactive oxygen species, leading to systematic oxidative stress, which is postulated to be a key mechanism of endothelial dysfunction and increased risk for cardiovascular disorders in patients with OSA. In this review, various biomarkers of oxidative stress, including high-sensitivity C-reactive protein, pregnancy-associated plasma protein-A, superoxide dismutase, cell-free DNA, 8-hydroxy-2-deoxyguanosine, advanced oxidation protein products, lipid peroxidation products, receptor for advanced glycation end-products, and thioredoxin are discussed. Biomarkers of oxidative stress have the potential to be used to assess disease severity and treatment response. Continuous positive airway pressure (CPAP) is one of the most common noninvasive treatments for OSA; it keeps the upper airways open during sleep. This reduces episodes of intermittent hypoxia, reoxygenation, and arousal at night. CPAP has been shown to have anti-inflammatory properties and decrease oxidative stress. The administration of certain compounds, like vitamins A, C, and E as well as N-acetylcysteine and allopurinol, can decrease oxidative stress markers. However, their role in the treatment of OSA remains unclear.

The Association Between Sleep Breathing Impairment Index and Cardiovascular Risk in Male Patients with Obstructive Sleep Apnea

“…Thus, only male OSA patients between 16 and 70 years old were enrolled. The exclusion criteria were (1) having received OSA treatment including continuous positive airway pressure (CPAP) before enrollment; (2) diagnosis of COPD, restless legs syndrome or narcolepsy; (3) pre-existing CVD, including coronary heart disease, stroke, peripheral vascular disease, or heart failure; (4) concurrent use of lipid-lowering medication or insulin; (5) severe chronic debilitating conditions or pregnancy; (6) inability to complete questionnaires; and (7) patients having total sleep time of <4 h. The study was approved by the ethics committees of PUMCH (JS-2632) and was conducted in accordance with the Declaration of Helsinki. Written informed consent was obtained from each participant in this study.…”

“…3,4 Besides, reactive oxide species induce endothelial dysfunction in the early stages of OSA by increasing the expression of leukocyte-specific and endothelial-specific adhesion molecules, and the endothelial dysfunction may also cause microvascular damage. 5 Additionally, OSA is linked with increased oxidative stress, which adversely affect the associated cardio-/cerebrovascular disease in OSA. 6 The adverse OSA effect on cardiovascular disease (CVD) has been well established.…”

Circulating Superoxide Dismutase Concentrations in Obstructive Sleep Apnoea (OSA): A Systematic Review and Meta-Analysis

“…Several studies investigated the concentrations of oxidant molecules in OSA patients, and their correlation with the severity of the disease [ 38 , 39 ]. A more limited number of studies have sought to elucidate the activity of key antioxidant enzymes, such as SOD and glutathione peroxidase [ 15 , 40 , 41 ]. SOD represents an important antioxidant mechanism in the detoxification of the superoxide anion, the most abundant ROS molecule [ 42 ].…”

“…While these studies generally reported correlations between some of these markers and the presence and severity of OSA, conflicting results exist regarding SOD concentrations in this group [ 14 ]. Furthermore, CPAP therapy, a fundamental treatment strategy in OSA also in view of its antioxidant effects, have shown to have little effect on SOD concentrations, in contrast to oxidative stress markers such as 8-isoprostane and 8-hydroxy-2-deoxyguanosine [ 15 ]. Therefore, in order to capture and critically appraise the available evidence on the pathophysiological role of SOD, we performed a systematic review and meta-analysis of studies reporting SOD concentrations in serum, plasma, and whole blood in OSA patients and non-OSA controls to detect possible differences between the two groups.…”

The Association of Nephroblastoma Overexpressed (NOV) and Endothelial Progenitor Cells with Oxidative Stress in Obstructive Sleep Apnea

“…Inflammation in OSA is driven by intermittent hypoxia and fragmented sleep leading to oxidative stress, manifested by increased formation of ROS and elevated adipocytokines [ 16 , 17 ]. Oxidative imbalance is the result of this intermittent hypoxia with increased inflammatory cytokine production of IL-6, TNF, and lipid peroxidation; literature review has not identified which biomarkers better correlate with the severity of disease [ 3 ].…”