scholarly journals Redox signaling via lipid peroxidation regulates retinal progenitor cell differentiation

2019 ◽  
Author(s):  
Shahad Albadri ◽  
Federica Naso ◽  
Carole Gauron ◽  
Carola Parolin ◽  
Karine Duroure ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Redox Signaling ◽  
Lipid Peroxidation Product ◽  
Histone Deacetylase 1 ◽  
Retinal Progenitor ◽  
Secondary Messengers ◽  
Fine Regulation ◽  
Peroxidation Product ◽  
Degradation Step

SummaryReactive oxygen species (ROS) and downstream products of lipid oxidation are emerging as important secondary messengers in tissue homeostasis. However their regulation and mechanism of action remain poorly studied in vivo during normal development. Here we reveal that the fine regulation of hydrogen peroxide (H2O2) levels at the degradation step by its scavenger Catalase is crucial to mediate the switch from proliferation to differentiation in retinal progenitor cells (RPCs). We further show that altering the levels of downstream products of the Redox signaling can also affect this switch. Indeed, we identify 9-hydroxystearic acid (9-HSA), an endogenous downstream lipid peroxidation product, as a mediator of this effect in the zebrafish retina. In fact, RPCs exposed to higher amounts of 9-HSA failed to differentiate and remained proliferative. We found that 9-HSA exerts its biological function in vivo by inhibiting the activity of histone deacetylase 1. We finally show that the local and temporal manipulation of H2O2 levels by catalase overexpression in RPCs was sufficient to trigger their premature differentiation. Therefore the amount of H2O2 in RPCs is instructive of their ability to switch from proliferation to differentiation. We propose a mechanism that acts in RPC and linking H2O2 homeostasis and neuronal differentiation via the modulation of lipid peroxidation.

scholarly journals Sensitivity of plant mitochondrial terminal oxidases to the lipid peroxidation product 4-hydroxy-2-nonenal (HNE)

2005 ◽  
Vol 387 (3) ◽  
pp. 865-870 ◽  
Author(s):  
Alison M. WINGER ◽  
A. Harvey MILLAR ◽  
David A. DAY
Keyword(s):  
Lipid Peroxidation ◽  
Cytochrome C ◽  
Cell Cultures ◽  
Cysteine Residue ◽  
Lipid Peroxidation Product ◽  
Amino Acid Residues ◽  
Peroxidation Product ◽  
High Concentrations ◽  
Transport In Mitochondria

We have investigated the effect of the lipid peroxidation product, HNE (4-hydroxy-2-nonenal), on plant mitochondrial electron transport. In mitochondria isolated from Arabidopsis thaliana cell cultures, HNE inhibited succinate-dependent oxygen consumption via the Aox (alternative oxidase), but had minimal effect on respiration via Cox (cytochrome c oxidase). Maximal Cox activity, measured with reduced cytochrome c as substrate, was only slightly inhibited by high concentrations of HNE, at which Aox was completely inhibited. Incubation with HNE prevented dimerization of the Aox protein, suggesting that one site of modification was the conserved cysteine residue involved in dimerization and activation of this enzyme (CysI). However, a naturally occurring isoform of Aox lacking CysI and unable to be dimerized, LeAox1b from tomato (Lycopersicon esculentum), was equally sensitive to HNE inhibition, showing that other amino acid residues in Aox also interact with HNE. The presence of HNE in vivo in Arabidopsis cell cultures was also investigated. Induction of oxidative stress in the cell cultures by the addition of hydrogen peroxide, antimycin A or menadione, caused a significant increase in hydroxyalkenals (of which HNE is the most prominent). Western blotting of mitochondrial proteins with antibodies against HNE adducts, demonstrated significant modification of proteins during these treatments. The implications of these results for the response of plants to reactive oxygen species are discussed.

Detection of the lipid peroxidation product malonaldehyde in rat brain in vivo

1995 ◽  
Vol 200 (1) ◽  
pp. 69-72 ◽  
Author(s):  
A.H. Waterfall ◽  
G. Singh ◽  
J.R. Fry ◽  
C.A. Marsden
Keyword(s):  
Lipid Peroxidation ◽  
Rat Brain ◽  
Lipid Peroxidation Product ◽  
Peroxidation Product

scholarly journals Interaction of 4-hydroxynonenal-modified low-density lipoproteins with the fibroblast apolipoprotein B/E receptor

1986 ◽  
Vol 234 (1) ◽  
pp. 245-248 ◽  
Author(s):  
W Jessup ◽  
G Jurgens ◽  
J Lang ◽  
H Esterbauer ◽  
R T Dean
Keyword(s):  
Apolipoprotein B ◽  
Negative Charge ◽  
Low Density Lipoprotein ◽  
Ldl Receptor ◽  
Density Lipoprotein ◽  
Low Density ◽  
Lipid Peroxidation Product ◽  
Modified Low Density Lipoproteins ◽  
Peroxidation Product

The incorporation of the lipid peroxidation product 4-hydroxynonenal into low-density lipoprotein (LDL) increases the negative charge of the particle, and decreases its affinity for the fibroblast LDL receptor. It is suggested that this modification may occur in vivo, and might promote atherogenesis.

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>

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