Abnormal lipid peroxidation in patients with sleep apnoea

Barceló, Antònia; Miralles, Cristina; Barbé, Ferrán; Vila, M.; Pons, Sebastián; Agustí, Àlvar

doi:10.1034/j.1399-3003.2000.16d13.x

Cited by 212 publications

(131 citation statements)

References 23 publications

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“…Barcelo et al [26] also reported that the lipid peroxidation profile is abnormal in OSA patients. Using LDL particles isolated from 14 patients with severe OSA (59 apnea/h) and 13 healthy subjects, they found that thiobarbituric acid-reactive substance (TBARS) formation was higher in OSA patients.…”

Section: Evidence For Oxidative Stress In Osa Patientsmentioning

confidence: 96%

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

Suzuki

Jain

Park

et al. 2006

Free Radical Biology and Medicine

203

123

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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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Section: Evidence For Oxidative Stress In Osa Patientsmentioning

confidence: 96%

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

Suzuki

Jain

Park

et al. 2006

Free Radical Biology and Medicine

203

123

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“…In particular, obese individuals with systemic hypoxemia (because of sleep-related breathing disorders including obstructive sleep apnea) may experience repeated bouts of hepatic hypoxia, hepatocyte necrosis, and ultimately develop NASH. Several pieces of evidence support the possibility that hypoxemia may play a role in pathogenesis of NASH: First, sleep disturbances and nocturnal hypoxemia are common in patients with NASH (Table 2); second, hypoxemia has been shown to alter the activity of different CYPs 27,28 ; third, sleep apnea and hypoxemia have been associated with lipid peroxidation and oxidative stress 29 ; and, fourth, in the dietary model of animal NASH 6 as well as the human study by Weltman et al, 8 CYP2E1 activity was most prominent in zone III, the least oxygenated area of the acinus. The significant association noted in this study between hepatic CYP2E1 activity and nocturnal hypoxemia is interesting.…”

Section: Discussionmentioning

confidence: 99%

Hepatic cytochrome P450 2E1 activity in nondiabetic patients with nonalcoholic steatohepatitis

et al. 2003

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Cytochrome P450 2E1 (CYP2E1) plays an important role in the pathogenesis of nonalcoholic steatohepatitis (NASH) in animal models, but its role in the pathogenesis of human NASH is unclear. Therefore, we measured hepatic CYP2E1 activity and its correlates in a cohort of nondiabetic patients with NASH (NDN) and controls to explore its role in the pathogenesis of human NASH. Hepatic CYP2E1 activity was assessed using the oral clearance (CL PO ) of chlorzoxazone (CHZ) in 20 NDN and 17 age, gender, and body mass index (BMI)-matched controls. The relationship between hepatic CYP2E1 activity and demographic and anthropometric variables; fasting levels of insulin, glucose, lipids, and ␤-OH butyrate; insulin resistance; and nocturnal hypoxemia was assessed. Furthermore, expression of CYP2E1 in the peripheral lymphocytes was assessed using reverse transcription-polymerase chain reaction (RT-PCR). The CL PO of CHZ was significantly (P ‫؍‬ .03) greater in NDN (41 ؎ 12 L/h) compared with controls (33 ؎ 16 L/h). Lymphocyte CYP2E1 messenger RNA was significantly higher in NDN compared with controls (11.5 ؋ 10 3 ؎ 10 ؋ 10 3 vs. 2.6 ؋ 10 3 ؎ 1.2 ؋ 10 3 molecules/ g total RNA, respectively, P < .001). On univariate analysis, BMI, respiratory quotient, high-density lipoprotein, triglycerides, insulin, insulin resistance, hypoxemia, and ␤-OH butyrate significantly correlated with hepatic CYP2E1 activity. However, on stepwise regression analysis, only nocturnal hypoxemia (r ‫؍‬ 0.50, P ‫؍‬ .009) and ␤-OH butyrate (r ‫؍‬ 0.37, P ‫؍‬ .04) were independent predictors of hepatic CYP2E1 activity. In conclusion, hepatic CYP2E1 activity and lymphocyte CYP2E1 expression are enhanced in NDN. The significant correlations noted between CYP2E1 and hypoxemia and ␤-OH butyrate suggest that these factors play a role in increased CYP2E1 activity that is seen in patients with NASH. (HEPATOLOGY 2003;37:544-550.)

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“…10 In addition, OSAHS has been found to be a factor involved in endothelial dysfunction, 11 infl ammation, 12 and sympathetic activation, which may promote ischemic events. Although an increased incidence of CAD has been found in patients with OSAHS, 13,14 and even mild to moderate OSAHS has been associated with a worse prognosis in patients with existing CAD, 15,16 the characterization of OSAHS in the acute myocardial ischemia setting is less clear. [17][18][19][20][21][22][23][24][25] Based on the results of recent studies 19,20,25 it is diffi cult to determine whether OSAHS contributes to the occurrence of ACS, or whether OSAHS is a consequence of the acute phase in ACS patients that may improve after medical stabilisation.…”

mentioning

confidence: 99%