Increased oxidative stress and decreased membrane fluidity in erythrocytes of CAD patients

Pytel, Edyta; Olszewska-Banaszczyk, Małgorzata; Koter−Michalak, Maria; Broncel, Marlena

doi:10.1139/bcb-2013-0027

Cited by 34 publications

(23 citation statements)

References 28 publications

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“…These are mainly composed of enzymes such as superoxide dismutases (SODs) and glutathione peroxidase (GPX), which scavenge the reactive oxygen species (ROS) produced by cellular metabolism. The process of coronary atherosclerosis is affected by these important enzymes [15]. SOD, which belongs to an enzyme family that is widely found in human cells and body fluids, protects cells against potential cytotoxicity by catalytically scavenging harmful superoxide radicals (O 2 − ).…”

Section: Introductionmentioning

confidence: 99%

Elevated Levels of Plasma Superoxide Dismutases 1 and 2 in Patients with Coronary Artery Disease

Chang

et al. 2016

BioMed Research International

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Aims. To measure plasma levels of superoxide dismutases 1, 2, and 3 (SOD1, 2, 3) and determine whether SODs can function as biomarkers for coronary artery disease (CAD). Patients & Methods. Patient groups were as follows: patients with stable angina pectoris (SAP, n = 33), patients with acute coronary syndrome (ACS, n = 49), and controls (n = 42). Protein quantification was done using ELISA. Results. The concentrations of plasma SOD1 and SOD2 were higher in CAD than in healthy controls. No difference in SOD3 levels between CAD and control groups was found. Limited correlations were found between SODs and gender, age, and severity of coronary artery stenosis. Conclusions. Plasma levels of SOD1 and SOD2 were elevated in patients with CAD and might serve as surrogate biomarkers for CAD.

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Section: Introductionmentioning

confidence: 99%

Elevated Levels of Plasma Superoxide Dismutases 1 and 2 in Patients with Coronary Artery Disease

Chang

et al. 2016

BioMed Research International

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“…MDA is a common general product of nonenzymatic peroxidation of polyunsaturated fatty and arachidonic acids. MDA may be increased in major depression (49) and in cardiovascular patients (15,59). Moreover, MDA is considered not only to be a product of lipid peroxidation but also known to be harmful for cell functions (1).…”

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confidence: 99%

Chronic selective serotonin reuptake inhibition modulates endothelial dysfunction and oxidative state in rat chronic mild stress model of depression

Matchkov

Кравцова

Wiborg

et al. 2015

American Journal of Physiology-Regulatory, Integrative and Comp

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Matchkov VV, Kravtsova VV, Wiborg O, Aalkjaer C, Bouzinova EV. Chronic selective serotonin reuptake inhibition modulates endothelial dysfunction and oxidative state in rat chronic mild stress model of depression. Am J Physiol Regul Integr Comp Physiol 309: R814 -R823, 2015. First published August 12, 2015 doi:10.1152/ajpregu.00337.2014.-Major depression is known to be associated with cardiovascular abnormalities, and oxidative stress has been suggested to play a role. We tested the hypothesis that antidepressant treatment reduces oxidative stress and endothelial dysfunctions in the chronic mild stress (CMS) model of depression in rats. Rats with Ͼ30% reduction in sucrose intake after 4 wk of CMS were defined in the study as CMS-susceptible and compared with unstressed controls. Sixteen CMS-susceptible and eight unstressed rats were treated during weeks 5 to 8 of the CMS protocol with escitalopram. Escitalopram-treated rats with Ͼ20% recovery in the sucrose consumption during the last 2 wk of treatment were defined as escitalopram responders. Rats that did not reach these criteria were defined as escitalopram nonresponders. In the open field test, escitalopram responders demonstrated anxiolytic effect of treatment. In mesenteric small arteries, escitalopram affected neither NO nor cyclooxygenase-1 (COX-1)-mediated vasodilation. Escitalopram potentiated endothelium-dependent hyperpolarization-like response, which was suppressed in the vehicle-treated CMS-susceptible rats and reduced COX-2-dependent relaxation, which was elevated in the vehicle-treated CMS-susceptible rats. Escitalopram did not affect blood pressure and heart rate, which were elevated in the vehicle-treated CMS-susceptible rats. Oxidative stress markers were changed in association with CMS in liver, heart, and brain. Escitalopram normalized oxidative stress markers in the majority of tissues. This study demonstrates that the antidepressant effect of escitalopram is associated with partial improvement of endothelial function in small arteries affecting COX-2 and endothelium-dependent hyperpolarization-like pathways.depression; chronic mild stress; escitalopram; endothelium; nitric oxide synthase; cyclooxygenase; endothelium-derived hyperpolarization; oxidative stress; glutathione; malondialdehyde CARDIOVASCULAR DISEASES AND major depressive disorder are the two most prevalent health problems in high-income countries (31). Their comorbidity is well recognized, but the mechanisms and critical factors underlying this comorbidity are unknown. Interactions between several factors common for both disorders are complex (17; 43). Thus, a dysfunction of the hypothalamic-pituitary-adrenal (HPA) axis and activation of the renin-angiotensin-aldosterone system lead to changes associated with both depression and cardiovascular abnormalities.Also dysfunction of the autonomic nervous system (sympathetic/parasympathetic) is known to be involved, as well as an activation of proinflammatory cytokines (46). Importantly, these factors can induce both depression and ch...

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“…The decreased activity of the antioxidative systems might be responsible for the increased peroxidation of membrane lipids or vice versa. However, it has been reported that increased peroxidation of membrane lipids causes a reduction in the activity of antioxidative enzymes [19,20].…”

Section: Discussionmentioning

confidence: 99%

Decreased Na+/K+-ATPase Activity and Altered Susceptibility to Peroxidation and Lipid Composition in the Erythrocytes of Metabolic Syndrome Patients with Coronary Artery Disease

et al. 2019

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Background: The increased generation of reactive oxygen species that occurs in the case of a metabolic syndrome (MetS) may be responsible for the increased oxidative injury to erythrocyte membranes in coronary artery disease (CAD). Therefore, we studied the effects of MetS on both indexes of oxidative damage and biochemical properties of erythrocyte membranes in CAD patients. Methods: We analyzed the markers of oxidative stress, Na⁺/K⁺-ATPase activity, total cholesterol content of erythrocyte membranes (CEM), and fatty acid compositions of the erythrocyte membrane in 82 patients with stable CAD and 39 non-CAD subjects. Results: The CAD patients had higher levels of CEM, membrane lipid peroxidation, erythrocyte superoxide dismutase (SOD) activity, and Na⁺/K⁺-ATPase activity compared with non-CAD subjects. The Na⁺/K⁺-ATPase activity was correlated negatively with membrane lipid peroxidation, and positively with the CEM. In CAD patients with MetS compared with those without MetS, we found that the membrane lipid peroxidation and CEM were increased, whereas the n-3 fatty acids content, SOD activity, Na⁺/K⁺-ATPase activity were decreased. Conclusion: These findings suggest an impairment of erythrocyte membrane biochemical properties in stable CAD patients as a consequence of oxidative injury that may contribute to the development of CAD. In addition, MetS may be related to increased oxidative injury to erythrocyte membranes.

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Increased oxidative stress and decreased membrane fluidity in erythrocytes of CAD patients

Cited by 34 publications

References 28 publications

Elevated Levels of Plasma Superoxide Dismutases 1 and 2 in Patients with Coronary Artery Disease

Elevated Levels of Plasma Superoxide Dismutases 1 and 2 in Patients with Coronary Artery Disease

Chronic selective serotonin reuptake inhibition modulates endothelial dysfunction and oxidative state in rat chronic mild stress model of depression

Decreased Na+/K+-ATPase Activity and Altered Susceptibility to Peroxidation and Lipid Composition in the Erythrocytes of Metabolic Syndrome Patients with Coronary Artery Disease

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