scholarly journals Early involvement of lysosome dysfunction in the degeneration of cerebral cortical neurons caused by the lipid peroxidation product 4-hydroxynonenal

2017 ◽  
Vol 140 (6) ◽  
pp. 941-954 ◽  
Author(s):  
Shi Zhang ◽  
Erez Eitan ◽  
Mark P. Mattson
Keyword(s):  
Lipid Peroxidation ◽  
Cortical Neurons ◽  
Lipid Peroxidation Product ◽  
Cerebral Cortical Neurons ◽  
Peroxidation Product

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>

Abstract 144: Role of Iron Metabolism on Outcomes after Cardiac Arrest and Resuscitation in Mice

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_4) ◽  
Author(s):  
Yusuke Miyazaki ◽  
Kei Hayashida ◽  
Takamitsu Ikeda ◽  
Eizo Marutani ◽  
Aranya Bagchi ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Cardiac Arrest ◽  
Cortical Neurons ◽  
Glucose Deprivation ◽  
Neurological Function ◽  
Lipid Peroxidation Product ◽  
Iron Loading ◽  
Intracellular Iron ◽  
Neurological Outcomes

Introduction: Ischemia and reperfusion (I/R) induces hepcidin in neurons and macrophages. Hepcidin downregulates ferroportin, the only known iron exporter, thereby inhibiting iron efflux and increases iron in ferroportin rich cells while decreasing serum iron. Increased intracellular iron after I/R induces ferroptosis, a regulated cell death characterized by iron-dependent lipid peroxidation. We hypothesized that hepcidin-induced sequestration of iron in neurons and macrophages, both of which express ferroportin, worsens post-cardiac arrest (CA) brain injury. Methods: Levels of hepcidin, iron, and a lipid peroxidation product, malondialdehyde; and expression of HAMP that encodes hepcidin, transferrin receptor 1, and markers of ferroptosis, PTGS2 and CHAC1, were measured in naïve and post-CA wild-type (WT) mice. To examine the effects of hepcidin on CA outcomes, hepcidin-deficient and WT mice were subjected to potassium-induced 8 min of CA followed by cardiopulmonary resuscitation (CPR). To determine the role of increased intracellular iron after CA/CPR, we administered iron-dextran (300 mg/kg IP) or vehicle to WT mice 24h before CA. The effect of liproxstatin-1, a ferroptosis inhibitor, on cell viability was assessed in murine primary cortical neurons after oxygen-glucose deprivation/reperfusion (OGD/R) with iron-loading. Results: Post-CA WT mice exhibited increased systemic HAMP expression, intracellular iron in spleen, and ferroptosis in brain. Hepcidin deficiency that decreases intracellular iron improved survival and neurological function after CA/CPR, whereas pre-arrest iron-loading that increases intracellular iron worsened survival and neurological function after CA/CPR (Fig. 1). Liproxstatin-1 improved neuron viability after OGD/R with iron-loading. Conclusions: Our data suggest that inhibiting hepcidin improves post-CA neurological outcomes by reducing intracellular iron and ferroptosis-induced neuronal death.

Metabolism of lipid peroxidation product, 4-hydroxynonenal (HNE) in rat erythrocytes: role of aldose reductase

2000 ◽  
Vol 29 (7) ◽  
pp. 642-651 ◽  
Author(s):  
Sanjay Srivastava ◽  
Bharat L Dixit ◽  
Jian Cai ◽  
Silky Sharma ◽  
Harrell E Hurst ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Aldose Reductase ◽  
Lipid Peroxidation Product ◽  
Rat Erythrocytes ◽  
Peroxidation Product

Identification of Novel Urinary Metabolites of the Lipid Peroxidation Product 4-Hydroxy-2-nonenal in Rats

1998 ◽  
Vol 11 (11) ◽  
pp. 1368-1376 ◽  
Author(s):  
Jacques Alary ◽  
Laurent Debrauwer ◽  
Yvette Fernandez ◽  
Alain Paris ◽  
Jean-Pierre Cravedi ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Urinary Metabolites ◽  
Lipid Peroxidation Product ◽  
Peroxidation Product
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