Total antioxidant status in patients with obstructive sleep apnea without comorbidities: the role of the severity of the disease

Katsoulis, K.; Kontakiotis, Theodoros; Spanogiannis, Dimitris; Vlachogiannis, Emmanouil; Kougioulis, Michalis N.; Gerou, Spyridon; Daskalopoulou, E. van Vliet

doi:10.1007/s11325-010-0456-y

Cited by 37 publications

(24 citation statements)

References 15 publications

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“…On the one hand, decreased total anti-oxidant status was described in adults with OSA compared to healthy controls and an inverse linear relationship between anti-oxidant capacity and AHI in adults was reported [48, 62]. However, others have observed lower total anti-oxidant levels in adults with mild to moderate but not severe OSA[63]. In the present study, lower serum alpha tocopherol and beta carotene normalized to total serum lipids were observed in NAFLD patients with OSA/hypoxia compared to lean controls.…”

Section: Discussionmentioning

confidence: 99%

Nocturnal hypoxia-induced oxidative stress promotes progression of pediatric non-alcoholic fatty liver disease

Sundaram

Halbower

Pan

et al. 2016

Journal of Hepatology

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Background Oxidative stress is proposed as a central mediator in NAFLD pathogenesis, but the specific trigger for reactive oxygen species generation has not been clearly delineated. In addition, emerging evidence shows that obesity-related obstructive sleep apnea (OSA) and nocturnal hypoxia are associated with NAFLD progression in adults. Aim To determine if OSA/nocturnal hypoxia induced oxidative stress promotes the progression of pediatric NAFLD. Methods Subjects with biopsy proven NAFLD and lean controls were studied. Subjects underwent polysomnograms, liver histology scoring, laboratory testing, urine F(2)-isoprostanes (measure of lipid peroxidation) and 4-hydroxynonenal liver immunohistochemistry (in situ hepatic lipid peroxidation). Results We studied 36 adolescents with NAFLD and 14 lean controls. The OSA/hypoxia group (69% of NAFLD subjects) had more severe fibrosis (64% Stage 0–2; 36 % Stage 3) than those without OSA/hypoxia (100% Stage 0–2), p=0.03. Higher F(2)-isoprostanes correlated with apnea/hypoxia index (r=0.39, p= 0.03), % time SaO2 <90% (r= 0.56, p=0.0008) and inversely with SaO2 nadir (r=−0.46, p=0.008). OSA/hypoxia was most severe in subjects with the greatest 4HNE staining (p=0.03). Increasing F(2)-isoprostanes(r=0.32, p=0.04) and 4HNE hepatic staining (r=0.47, p=0.007) were associated with worsening steatosis. Greater oxidative stress occurred in subjects with definite NASH as measured by F(2)-isoprostanes (p=0.06) and hepatic 4HNE (p=0.03) compared to those with borderline/not NASH. Conclusions These data support the role of nocturnal hypoxia as a trigger for localized hepatic oxidative stress, an important factor associated with the progression of NASH and hepatic fibrosis in obese pediatric patients.

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Section: Discussionmentioning

confidence: 99%

Nocturnal hypoxia-induced oxidative stress promotes progression of pediatric non-alcoholic fatty liver disease

Sundaram

Halbower

Pan

et al. 2016

Journal of Hepatology

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“…Yamauchi et al [39] found increased urinary 8-hydroxy-20-deoxyguanosine (8-OhdG) excretion in the severe OSA patients, Carpagnano et al [10] observed elevated 8-isoprostane levels in the exhaled breath condensate in OSA patients and Dyugovskaya et al [40] detected an increase in the production of ROS in OSA. Several other studies reported abnormal lipid peroxidation in OSAS [7,8] or reduced total antioxidant status [9]. Conversely, Wali et al [41] found no differences in susceptibility of LDL to oxidative stress and Svatikova et al [42] reported that patients with moderate – severe OSA did not have evidence for greater oxidative stress and lipid peroxidation than healthy normal subjects.…”

Section: Discussionmentioning

confidence: 99%

Oxidative stress mediated arterial dysfunction in patients with obstructive sleep apnoea and the effect of continuous positive airway pressure treatment

et al. 2012

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BackgroundSeveral studies suggest an increase of oxidative stress and a reduction of endothelial function in obstructive sleep apnoea syndrome (OSAS). We assessed the association between OSAS, endothelial dysfunction and oxidative stress. Further aim was to evaluate the effect of nasal continuous positive airway pressure (nCPAP) on oxidative stress and arterial dysfunction.MethodsWe studied 138 consecutive patients with heavy snoring and possible OSAS. Patients underwent unattended overnight home polysomnography. Ten patients with severe OSAS were revaluated after 6 months of nCPAP therapy. To assess oxidative stress in vivo, we measured urinary 8-iso-PGF2α and serum levels of soluble NOX2-derived peptide (sNOX2-dp). Serum levels of nitrite/nitrate (NOx) were also determined. Flow-mediated brachial artery dilation (FMD) was measured to asses endothelial function.ResultsPatients with severe OSAS had higher urinary 8-iso-PGF2α (p<0.001) and serum NOX2 and lower NOx. A negative association was observed between FMD and OSA severity. Apnea/hypopnea index was significantly correlated with the indices of central obesity and with urinary 8-isoprostanes (r=0.298, p<0.001). The metabolic syndrome (t=-4.63, p<0.001) and urinary 8-isoprostanes (t=-2.02, p<0.05) were the only independent predictors of FMD. After 6-months nCPAP treatment, a significant decrease of serum NOX2, (p<0.005) and urinary 8-iso-PGF2α (p<0.01) was observed, while serum NOx showed only a minor increase. A statistically significant increase of FMD was observed (from 3.6% to 7.0%).ConclusionsThe results of our study indicate that patients with OSAS and cardiometabolic comorbidities have increased oxidative stress and arterial dysfunction that are partially reversed by nCPAP treatment.

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“…On the other hand, Katsoulis et al reported some unexpected results where they found that total antioxidant status before and after sleep was significantly lower in OSA patients with AHI < 30 (1.73 versus 1.65 mmol/L, P = 0.01) but not in severe OSA patients with AHI > 30 (1.64 versus 1.58 mmol/L, P = 0.07). A possible explanation could be due to differences between the acute effects of hypoxia resulting from apneic sleep and chronic oxidative stress that may be sustained in severe OSA patients even during the daytime [53]. …”

Section: Oxidative Stress In Osamentioning

confidence: 99%

Cardiovascular Complications of Sleep Apnea: Role of Oxidative Stress

Badran

Ayas

Laher

2014

Oxidative Medicine and Cellular Longevity

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Obstructive sleep apnea (OSA) occurs in 2% of middle-aged women and 4% of middle-aged men with a higher prevalence among obese subjects. This condition is considered as an independent risk factor for cerebrovascular and cardiovascular diseases. One of the major pathophysiological characteristics of OSA is intermittent hypoxia. Hypoxia can lead to oxidative stress and overproduction of reactive oxygen species, which can lead to endothelial dysfunction, a hallmark of atherosclerosis. Many animal models, such as the rodent model of intermittent hypoxia, mimic obstructive sleep apnea in human patients and allow more in-depth investigation of biological and cellular mechanisms of this condition. This review discusses the role of oxidative stress in cardiovascular disease resulting from OSA in humans and animal models.

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Total antioxidant status in patients with obstructive sleep apnea without comorbidities: the role of the severity of the disease

Cited by 37 publications

References 15 publications

Nocturnal hypoxia-induced oxidative stress promotes progression of pediatric non-alcoholic fatty liver disease

Nocturnal hypoxia-induced oxidative stress promotes progression of pediatric non-alcoholic fatty liver disease

Oxidative stress mediated arterial dysfunction in patients with obstructive sleep apnoea and the effect of continuous positive airway pressure treatment

Cardiovascular Complications of Sleep Apnea: Role of Oxidative Stress

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