Abstract 5702: Oxidative Stress in Patients with Lone Atrial Fibrillation

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Kengo Kusano ◽  
Kazufumi Nakamura ◽  
Tohru Ohe
Keyword(s):  
Oxidative Stress ◽  
Atrial Fibrillation ◽  
Immunohistochemical Analysis ◽  
Lipid Peroxidation Product ◽  
Lone Atrial Fibrillation ◽  
Activated T Cells ◽  
Mhc I ◽  
Mhc Ii ◽  
Peroxidation Product ◽  
Ros Formation

Background: Lone atrial fibrillation (LAF) is a common arrhythmia, but its mechanism and the aggravated factor of arrhythmia are poorly understood. Oxidative stress has been implicated in the pathogenesis of heart failure. We have previously demonstrated that the amount of 4-hydroxy-2-nonenal (HNE) modified protein, which is a major lipid peroxidation product and a cytotoxic aldehyde, causes intracellular Ca2+ overload via reactive oxygen species (ROS) formation in cardiomyocytes and leads to develop arrhythmia. Accordingly we examined the levels of HNE and major histocompatibility complex (MHC) with the disease severity in LAF patients. Method: Atrial and ventricular myocardial samples were obtained from twelve patients (11 men and 1 woman, mean 48±14 years old) by endomyocardial biopsy in 10, autopsy sample in 1 and surgical resection sample in 1. Histological assessments and immunohistochemical analysis for HNE modified protein, MHC class-I and -II antigens (grade 0 to 3) were performed and compared with LAF severity. Results: Histological assessment showed that increased number of interstitial cells (mainly activated T cells) was observed only in the atrium but not in the ventricle. Moderate to severe expression of MHC antigens (grade 2 or 3) was more observed in the atrium than the ventricle (MHC-I: seven in atrium and three in ventricle; MHC-II: ten in atrium and four in ventricle). Atrial myocarditis was detected in 6 out of 11 samples. HNE modified protein was also more observed in the atrium than that in the ventricle. In addition, more severe expression of HNE staining was observed in the samples from persistent/chronic LAF than that in paroxysmal LAF. Conclusion: These data indicates that oxidative stress plays an important role as an aggravating factor in LAF patients.

scholarly journals Carotid intima-media thickness and oxidative stress markers for assessment of atherosclerosis in children with β thalassemia major

2016 ◽  
Vol 6 (1) ◽  
Author(s):  
Geetanjali Jindal ◽  
Prashant Chavan ◽  
Ravinder Kaur ◽  
Shivani Jaswal ◽  
Kamal Kumar Singhal ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Oxidized Ldl ◽  
Thalassemia Major ◽  
Lipid Peroxidation Product ◽  
Oxidative Stress Markers ◽  
Lipoprotein A ◽  
Stress Markers ◽  
Total Antioxidant ◽  
Peroxidation Product

<p>The present study evaluates carotid intimamedia thickness (CIMT) in children with β thalassemia major to assess atherosclerosis and its relation to the underlying proposed causative mechanisms <em>via</em> lipid peroxidation product malondialdehyde (MDA), oxidized lowdensity lipoproteins (LDL), total antioxidant level, and lipid profile. A cross sectional study was conducted on 62 children (31 cases and 31 controls). CIMT by high resolution ultrasound and biochemical parameters <em>i.e.</em>, total cholesterol, triglycerides, high-density lipoproteins, LDL, Oxidized LDL, lipoprotein (a), lipid peroxidation product MDA and total antioxidant were measured in enrolled subjects and compared. In our study, CIMT was significantly increased in β thalassemia major patients’ as compared to healthy controls. Mean CIMT in cases was 0.69±0.11 mm and in controls 0.51±0.07 mm. Mean oxidized LDL (EU/mL) in cases 39.3±34.4 (range 14.4 to 160) was significantly raised (P=0.02, t test) as compared to controls 23.9±13.4 (range 12 to 70). In our study we found MDA levels (nmol/mL) to be increased in β thalassemia patients as compared to controls. Mean MDA was 10.0±3.27 (4.41 to 17.48) in cases while in controls was 6.87±4.55 (1.5 to 17.9). Our study results show CIMT as an early marker of atherogenesis in β thalassemia major. Oxidative stress markers are also increased in β thalassemia major patients and lipoprotein (a) shows a positive correlation with CIMT. The present study points towards various atherogenetic mechanisms in β thalassemia major.</p><p> </p><p>本研究评价β重型地中海贫血患儿颈动脉内膜中层厚度（CIMT），以评估动脉粥样硬化，以及与潜在通过血脂过氧化反应产物丙二醛（MDA）、氧化低密度脂蛋白（LDL）、总抗氧化水平和血脂谱所提出致病机制之间的关系。 在62名儿童（31例病例和31例对照）中进行了一项横断面研究。 在入组受试者中通过高分辨率超声和生化指标（即总胆固醇、甘油三酯、高密度脂蛋白、LDL、氧化LDL，脂蛋白（a）、血脂过氧化产物MDA和总抗氧化剂）测量CIMT并进行比较。 在我们的研究中，CIMT在β重型地中海贫血患者中比健康对照组显著增加。 病例组中的平均CIMT为0.69±0.11 mm，对照组0.51±0.07 mm。病例组中平均氧化LDL（EU/mL）为39.3±34.4（从14.4到160的范围）与对照组的23.9±13.4（12至70的范围）相比显著升高（P = 0.02，t检验）。 在我们的研究中，我们发现β地中海贫血患者中的MDA水平（nmol/mL）比对照组更高。 病例组中的平均MDA为10.0±3.27（4.41至17.48），而对照组为6.87±4.55（1.5到17.9）。 我们的研究结果表明，CIMT是β重型地中海贫血动脉粥样硬化的早期标记物。 氧化应激标记物在β重型地中海贫血患者中也有增加，脂蛋白（a）显示出与CIMT呈正相关。 本研究针对β重型地中海贫血中的各种动脉粥样硬化机制。</p>

scholarly journals Reducing sugars trigger oxidative modification and apoptosis in pancreatic β-cells by provoking oxidative stress through the glycation reaction

1996 ◽  
Vol 320 (3) ◽  
pp. 855-863 ◽  
Author(s):  
Hideaki KANETO ◽  
Junichi FUJII ◽  
Theingi MYINT ◽  
Nobuko MIYAZAWA ◽  
Kazi N. ISLAM ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Dna Cleavage ◽  
Reducing Sugars ◽  
Islet Cells ◽  
Chromatin Condensation ◽  
Oxidative Modification ◽  
Lipid Peroxidation Product ◽  
Β Cells ◽  
Pancreatic Β Cells ◽  
Peroxidation Product

Several reducing sugars brought about apoptosis in isolated rat pancreatic islet cells and in the pancreatic β-cell-derived cell line HIT. This apoptosis was characterized biochemically by internucleosomal DNA cleavage and morphologically by nuclear shrinkage, chromatin condensation and apoptotic body formation. N-Acetyl-l-cysteine, an antioxidant, and aminoguanidine, an inhibitor of the glycation reaction, inhibited this apoptosis. We also showed directly that proteins in β-cells were actually glycated by using an antibody which can specifically recognize proteins glycated by fructose, but not by glucose. Furthermore, fluorescence-activated cell sorting analysis using dichlorofluorescein diacetate showed that reducing sugars increased intracellular peroxide levels prior to the induction of apoptosis. Levels of carbonyl, an index of oxidative modification, and of malondialdehyde, a lipid peroxidation product, were also increased. Taken together, these results suggest that reducing sugars trigger oxidative modification and apoptosis in pancreatic β-cells by provoking oxidative stress mainly through the glycation reaction, which may explain the deterioration of β-cells under conditions of diabetes.

scholarly journals Fumonisin B1 Induces Oxidative Stress and Breaks Barrier Functions in Pig Iliac Endothelium Cells

Toxins ◽  
2019 ◽  
Vol 11 (7) ◽  
pp. 387 ◽  
Author(s):  
Qiaoling Yuan ◽  
Yancheng Jiang ◽  
Ying Fan ◽  
Yingfeng Ma ◽  
Hongyu Lei ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Fumonisin B1 ◽  
Thioredoxin Reductase ◽  
Lipid Peroxidation Product ◽  
Barrier Functions ◽  
Feed Material ◽  
Peroxidation Product ◽  
Endothelium Cells ◽  
Main Component

Fumonisins (Fums) are types of mycotoxin that widely contaminante feed material crops, and can trigger potential biological toxicities to humans and various animals. However, the toxicity of Fums on porcine blood vessels has not been fully explored. Fumonisin B1 (FB1) is the main component of Fums. Therefore, the aim of this study was to explore the effects of FB1 on the oxidative stress and tight junctions of the pig iliac endothelial cells (PIECs) in vitro. The results showed that FB1 reduced the viability of PIECs, increased the contents of lipid peroxidation product malondialdehyde (MDA), decreased the activities of antioxidant enzymes superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), catalase (CAT) and thioredoxin reductase (TrxR), and decreased the level of glutathione (GSH). In addition, the barrier functions were destroyed, along with the down-regulations on Claudin 1, Occludin and ZO-1 and the increase of paracellular permeability. Thus, this research indicates that FB1 facilitates oxidative stress and breaks barrier functions to damage pig iliac endothelium cells.

scholarly journals Intensification of Doxorubicin-Related Oxidative Stress in the Heart by Hypothyroidism Is Not Related to the Expression of Cytochrome P450 NADPH-Reductase and Inducible Nitric Oxide Synthase, As Well As Activity of Xanthine Oxidase

2012 ◽  
Vol 2012 ◽  
pp. 1-11 ◽  
Author(s):  
Jaroslaw Dudka ◽  
Franciszek Burdan ◽  
Agnieszka Korga ◽  
Magdalena Iwan ◽  
Barbara Madej-Czerwonka ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cytochrome P450 ◽  
Xanthine Oxidase ◽  
Lipid Peroxidation Product ◽  
Glutathione Level ◽  
Oxidative Damages ◽  
Peroxidation Product ◽  
Oxide Synthase ◽  
Doxorubicin Administration ◽  
Inducible Nitric Oxide

Cytochrome P450 NADPH-reductase (P450R), inducible synthase (iNOS) and xanthine oxidase play an important role in the antracycline-related cardiotoxicity. The expression of P450R and iNOS is regulated by triiodothyronine. The aim of this study was to evaluate the effect of methimazole-induced hypothyreosis on oxidative stress secondary to doxorubicin administration. 48 hours after methimazole giving cessation, rats were exposed to doxorubicin (2.0, 5.0 and 15 mg/kg). Blood and heart were collected 4, 48 and 96 h after the drug administration. Animals exposed exclusively to doxorubicin or untreated ones were also assessed. The hypothyreosis (0.025% of methimazole) significantly increased the doxorubicin effect on the cardiac carbonyl group and they may increase the glutathione level. An insignificant effect of methimazole was noticed in case of the cardiac lipid peroxidation product, the amount of DNA oxidative damages, iNOS and xanthine oxidase-enzymes responsible for red-ox activation of doxorubicin. However, the concentration of P450R was affected by a lower dose of methimazole in rats administered with doxorubicin. Since in rats receiving doxorubicin changes in oxidative stress caused by methimazole were not accompanied by elevation of bioreductive enzymes, it may be concluded that these changes in the oxidative stress were not related to the tested enzymes.

scholarly journals Dexmedetomidine Analgesia Effects in Patients Undergoing Dental Implant Surgery and Its Impact on Postoperative Inflammatory and Oxidative Stress

2015 ◽  
Vol 2015 ◽  
pp. 1-11 ◽  
Author(s):  
Sisi Li ◽  
Yang Yang ◽  
Cong Yu ◽  
Ying Yao ◽  
Yujia Wu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Postoperative Analgesia ◽  
Plasma Levels ◽  
Lipid Peroxidation Product ◽  
Necrosis Factor Alpha ◽  
Pain Scores ◽  
Dental Implantation ◽  
Peroxidation Product ◽  
Group D ◽  
And Oxidative Stress

The aim of the study was to determine whether or not dexmedetomidine- (DEX-) based intravenous infusion in dental implantation can provide better sedation and postoperative analgesia via suppressing postoperative inflammation and oxidative stress. Sixty patients were randomly assigned to receive either DEX (group D) or midazolam (group M). Recorded variables were vital sign (SBP/HR/RPP/SpO2/RR), visual analogue scale (VAS) pain scores, and observer’s assessment of alertness/sedation scale (OAAS) scores. The plasma levels of interleukin-6 (IL-6), tumor necrosis factor alpha (TNF-α), antioxidant superoxide dismutase (SOD), and the lipid peroxidation product malondialdehyde (MDA) were detected at baseline and after 2, 4, and 24 h of drug administration. The VAS pain scores and OAAS scores were significantly lower for patients in group D compared to group M. The plasma levels of TNF-α, IL-6, and MDA were significantly lower in group D patients than those in group M at 2 h and 4 h. In group M, SOD levels decreased as compared to group D at 2 h and 4 h. The plasma levels of TNF-α, IL-6, and MDA were positively correlated with VAS pain scores while SOD negatively correlated with VAS pain scores. Therefore, DEX appears to provide better sedation during office-based artificial tooth implantation. DEX offers better postoperative analgesia via anti-inflammatory and antioxidation pathway.

Determination of Relationship Between Lipid Peroxidation, Antioxidant Defence, Trace Elements and Hemorheology in COPD

2018 ◽  
Author(s):  
Devrim Saribal ◽  
F Sinem Hocaoglu-Emre ◽  
Birsen Aydemir ◽  
Mehmet Can Akyolcu
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Trace Elements ◽  
Blood Viscosity ◽  
Lipid Peroxidation Product ◽  
Serum Concentrations ◽  
Copd Patients ◽  
Significant Difference ◽  
Anti Oxidant ◽  
Peroxidation Product

Background and objective: Oxidative stress has important role in pathogenesis of chronic obstructive pulmonary disease (COPD). There are studies suggesting the role of increased oxidative stress and decreased antioxidants in COPD patients. The aim of this study was to assess the levels of oxidative and anti-oxidant system elements, serum concentrations of trace elements and blood viscosity in COPD patients. Methods: Our study group consisted of 25 male patients with COPD, and 25 healthy non-smokers. The lipid peroxidation product malondialdehyde (MDA) and anti-oxidant system elements superoxide dismutase (SOD), Catalase (CAT) and Glutathione (GSH) were measured spectrophotometrically. Serum concentrations of Copper (Cu), Zinc (Zn) and Iron (Fe) were determined using an atomic absorption spectrophotometer. Additionally, we measured blood viscosity using a viscosimeter. Results: Lipid peroxidation product MDA levels were found to be higher in plasma and erythrocytes. However GSH levels, SOD and Catalase enzyme activities were lower in erythrocytes of patient group than that of controls (p&lt;0,01). Fe and Zn levels were decreased, whereas Cu levels were increased in patient samples (p&lt;0,05; p&lt;0,01, respectvely). There was no statistically significant difference between plasma and blood viscosities. Conclusions: The results of this study indicate that COPD leads to the lipid peroxidation in erythrocyte membrane, and decreased levels of anti-oxidant system elements. Serum trace element concentrations were found to be altered in COPD patients, suggesting their interaction with oxidant and anti-oxidant enzymes.

scholarly journals Influence of Iron on Cytotoxicity and Gene Expression Profiles Induced by Arsenic in HepG2 Cells

2019 ◽  
Vol 16 (22) ◽  
pp. 4484
Author(s):  
Yonghua Wang ◽  
Yuxuan Liu ◽  
Su Liu ◽  
Bing Wu
Keyword(s):  
Oxidative Stress ◽  
Gene Expression ◽  
Hepg2 Cells ◽  
Expression Profiles ◽  
Gene Expression Profiles ◽  
Interactive Effects ◽  
Lipid Peroxidation Product ◽  
Biological Processes ◽  
Mitochondrial Depolarization ◽  
Peroxidation Product

The toxicity of arsenic (As) could be influenced by many environmental factors and elements. Iron (Fe) is one of the elements that could be involved in As-induced toxicity. In this study, the interactive effects of Fe and As in HepG2 cells were analyzed based on cytotoxicity and transcriptomic analyses. The results showed that Fe could decrease cell viability and increase mitochondrial depolarization induced by As exposure. Oxidative stress and damage have been proven to be one of the main mechanisms of As toxicity. Our results showed that Fe increased the generation of reactive oxygen species (ROS) and lipid peroxidation product malondialdehyde (MDA) induced by As exposure. Microarray analysis further verified that Fe increased the alteration of gene expression and biological processes related to oxidative stress, cell proliferation, and the apoptotic signaling pathway caused by As exposure. Both results of cytotoxicity and transcriptomic analyses suggest that an increase of Fe in the human body could increase the As-induced toxicity, which should be considered during the health risk assessment of As.

scholarly journals Can Medicinal Plants and Bioactive Compounds Combat Lipid Peroxidation Product 4-HNE-Induced Deleterious Effects?

Biomolecules ◽  
2020 ◽  
Vol 10 (1) ◽  
pp. 146 ◽  
Author(s):  
Fei-Xuan Wang ◽  
Hong-Yan Li ◽  
Yun-Qian Li ◽  
Ling-Dong Kong
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Medicinal Plants ◽  
Bioactive Compounds ◽  
Lipid Peroxidation Product ◽  
Metabolism Disorder ◽  
Human Disorders ◽  
Eye Damage ◽  
Peroxidation Product ◽  
Energy Metabolism Disorder

The toxic reactive aldehyde 4-hydroxynonenal (4-HNE) belongs to the advanced lipid peroxidation end products. Accumulation of 4-HNE and formation of 4-HNE adducts induced by redox imbalance participate in several cytotoxic processes, which contribute to the pathogenesis and progression of oxidative stress-related human disorders. Medicinal plants and bioactive natural compounds are suggested to be attractive sources of potential agents to mitigate oxidative stress, but little is known about the therapeutic potentials especially on combating 4-HNE-induced deleterious effects. Of note, some investigations clarify the attenuation of medicinal plants and bioactive compounds on 4-HNE-induced disturbances, but strong evidence is needed that these plants and compounds serve as potent agents in the prevention and treatment of disorders driven by 4-HNE. Therefore, this review highlights the pharmacological basis of these medicinal plants and bioactive compounds to combat 4-HNE-induced deleterious effects in oxidative stress-related disorders, such as neurotoxicity and neurological disorder, eye damage, cardiovascular injury, liver injury, and energy metabolism disorder. In addition, this review briefly discusses with special attention to the strategies for developing potential therapies by future applications of these medicinal plants and bioactive compounds, which will help biological and pharmacological scientists to explore the new vistas of medicinal plants in combating 4-HNE-induced deleterious effects.

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