Structural and Electronic Variations of sp/sp2 Carbon-Based Bridges in Di- and Trinuclear Redox-Active Iron Complexes Bearing Fe(diphosphine)2X (X = I, NCS) Moieties

2015 ◽  
Vol 34 (2) ◽  
pp. 408-418 ◽  
Author(s):  
Franziska Lissel ◽  
Olivier Blacque ◽  
Koushik Venkatesan ◽  
Heinz Berke
Keyword(s):  
Iron Complexes ◽  
Active Iron ◽  
Redox Active ◽  
Carbon Based

In vitro study on the effects of iron sucrose, ferric gluconate and iron dextran on redox-active iron and oxidative stress

2011 ◽  
Vol 60 (07) ◽  
pp. 459-465
Author(s):  
Brigitte Sturm ◽  
Hannes Steinkellner ◽  
Nina Ternes ◽  
Hans Goldenberg ◽  
Barbara Scheiber-Mojdehkar
Keyword(s):  
Oxidative Stress ◽  
In Vitro Study ◽  
Iron Sucrose ◽  
Vitro Study ◽  
Iron Dextran ◽  
Active Iron ◽  
Redox Active ◽  
And Oxidative Stress

Abstract T P351: Unbound Iron and Ceruloplasmin Levels in Cerebrospinal Fluid Are Associated with Development of Deep Cerebral Infarcts Following Subarachnoid Hemorrhage

Stroke ◽  
2014 ◽  
Vol 45 (suppl_1) ◽  
Author(s):  
Lauren Koffman ◽  
Gabor Toth ◽  
M. Shazam Hussain ◽  
Magdy Selim ◽  
Peter Rasmussen ◽  
...  
Keyword(s):  
Cerebrospinal Fluid ◽  
Subarachnoid Hemorrhage ◽  
Cerebral Infarcts ◽  
Active Iron ◽  
Redox Active ◽  
Wilcoxon Rank Sum Test ◽  
Radiological Data ◽  
Experimental Subarachnoid Hemorrhage ◽  
Preliminary Study ◽  
Iron Redox

Introduction: Iron-dependent formation of reactive oxygen species has been implicated in the development of vasospasm (VSP) and neuronal injury following experimental subarachnoid hemorrhage (SAH). We report the association between unbound (“free”) iron in CSF of SAH patients and the risk of angiographic vasospasm and cerebral infarcts (CI) on neuroimaging from a recently completed pilot study. Methods: Samples of cerebrospinal fluid (CSF) were obtained on days 1, 3, and 5. A fluorometric assay that relies on an oxidation sensitive probe was used to measure redox active iron (REDOX-Fe). Ceruloplasmin (Cp) concentration and levels of malondialdehyde (MDA), a marker of lipid peroxidation were also measured. We prospectively collected and recorded demographic, clinical, and radiological data. Logistic regression and Wilcoxon Rank Sum test were used. Results: Five of 12 patients developed angiographic VSP (41.6%) and eight developed CI (66.6%). Mean REDOX-Fe was higher in patients with CI (3.96 ± 0.97 Vs. 2.77 ± 0.87 mcg/dl, p 0.07), particularly in patients with deep-seated strokes (4.56 ± 0.67 Vs. 3.35 ± 0.89, p 0.03). Levels of Cp at day 3 were lower in patients with deep strokes (34,092 ± 23,780 Vs. 86,045 ± 34,752 ng/ml, p 0.03). A trend towards higher REDOX-Fe on day 3 in patients who developed VSP (4.52 ± 1.16 Vs. 2.96 ± 0.71, p 0.07), and lower Cp levels on day 5 (45,033 ± 29,079 Vs. 63,044 ± 24,821, p 0.1) was found. Levels of MDA were higher in patients who developed CI (10.36 ± 4.36 Vs. 5.9 ± 4.2 nmol, p 0.08). Conclusions: In this preliminary study we found higher concentrations of redox active iron in CSF of SAH patients who develop deep-seated CI on neuroimaging. Evidence of increased oxidative damage correlated with development of CI. A possible association between non-protein bound iron and angiographic VSP is suggested as well. Ceruloplasmin may exert a protective effect in this setting. Further studies are needed to validate these findings.

199 Red Cell Rejuvenation Targets Inflammatory Microparticles, free Haemoglobin and Redox Active Iron: Key Mediators of Transfusion Related Acute Lung Injury in Cardiac Surgery

Heart ◽  
2015 ◽  
Vol 101 (Suppl 4) ◽  
pp. A110.2-A110
Author(s):  
Saqib Qureshi ◽  
Nishith Patel ◽  
Marcin Wozniak ◽  
Rebecca Cardigan ◽  
Gavin Murphy
Keyword(s):  
Cardiac Surgery ◽  
Acute Lung Injury ◽  
Lung Injury ◽  
Red Cell ◽  
Active Iron ◽  
Redox Active ◽  
Free Haemoglobin

Synthesis and Catalysis of Redox-Active Bis(imino)acenaphthene (BIAN) Iron Complexes

ChemCatChem ◽  
2017 ◽  
Vol 9 (16) ◽  
pp. 3203-3209 ◽  
Author(s):  
Matteo Villa ◽  
Dominique Miesel ◽  
Alexander Hildebrandt ◽  
Fabio Ragaini ◽  
Dieter Schaarschmidt ◽  
...  
Keyword(s):  
Iron Complexes ◽  
Redox Active

Exogenous intracellular, but not extracellular, iron augments myocardial reperfusion injury

1994 ◽  
Vol 266 (2) ◽  
pp. H384-H392 ◽  
Author(s):  
E. J. Lesnefsky ◽  
J. Ye
Keyword(s):  
Myocardial Injury ◽  
Lipid Peroxide ◽  
Oxidative Injury ◽  
Early Reperfusion ◽  
Excess Iron ◽  
Active Iron ◽  
Direct Demonstration ◽  
Redox Active ◽  
Catalyzed Reactions ◽  
Developed Pressure

Although previous studies using iron chelators suggest that iron-catalyzed reactions exacerbate myocardial injury, a direct demonstration of the timing, sites, and mechanisms of iron-mediated damage during reperfusion has been lacking. Catalytic doses of redox-active iron react with exogenously administered oxygen radical-generating systems to exacerbate myocardial injury. In an analogous manner, catalytic doses (5 microM) of excess iron present during early reperfusion should augment oxidative injury, if the redox-active iron is present in the same compartment as both the oxygen radicals generated during reperfusion as well as the critical biochemical targets of oxidative injury. We determined whether catalytic doses of iron given during early reperfusion could exacerbate myocardial injury and whether iron-catalyzed injury required intra- or extracellular iron. Buffer-perfused rabbit hearts underwent 30 min of 37 degrees C global ischemia and 30 min of reperfusion. Iron (5 microM), attached to ligands that either restrict iron to the extracellular space (ADP) or facilitate the entry of iron into myocytes (omadine, tropolone), was infused during the last 3 min of ischemia and the first 4 min of reperfusion. Recovery of developed pressure was decreased (P < 0.05) in omadine-iron and tropolone-iron compared with ADP-iron and noniron hearts treated with ligands alone. Tissue lipid peroxide levels, an index of oxidative injury, were increased (P < 0.05) by omadine-iron and tropolone-iron, but not ADP-iron. The oxidative damage caused by omadine-iron was blocked by pretreatment with dimethylthiourea, a cell-permeable scavenger of the hydroxyl radical.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Neuromelanin associated redox-active iron is increased in the substantia nigra of patients with Parkinson's disease

2003 ◽  
Vol 86 (5) ◽  
pp. 1142-1148 ◽  
Author(s):  
Baptiste A. Faucheux ◽  
Marie-Elise Martin ◽  
Carole Beaumont ◽  
Jean-Jacques Hauw ◽  
Yves Agid ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Substantia Nigra ◽  
Active Iron ◽  
Redox Active

Oxidative Stress and Vaso-Occlusion in Sickle Cell Disease: Role of Activated Leukocytes and Redox Active Iron.

Blood ◽  
2005 ◽  
Vol 106 (11) ◽  
pp. 3165-3165 ◽  
Author(s):  
John D. Belcher ◽  
Hemachandra Mahaseth ◽  
Thomas E. Welch ◽  
Felix Boakye-Agyeman ◽  
Robert P. Hebbel ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Sickle Cell Disease ◽  
Blood Cell ◽  
Sickle Cell ◽  
Ambient Air ◽  
Acute Chest Syndrome ◽  
Cell Disease ◽  
Active Iron ◽  
Redox Active ◽  
Hypoxia Reoxygenation

Abstract Sickle cell disease (SCD) is a disease of oxidative stress. We and others have demonstrated increased oxidative stress, inflammation, endothelial cell activation and white blood cell counts in human patients and transgenic murine models of SCD. Leukocytosis in SCD is associated with increases in the incidence of pain crisis, acute chest syndrome, stroke and mortality. We hypothesize that reactive oxygen species (ROS) derived from leukocytes and excess redox active iron promote vascular inflammation and vaso-occlusion. Leukocytes were activated in S+S-Antilles sickle mice compared to normal C57BL/6 control mice as measured by the percentage of leukocytes expressing CD11b on their surface in ambient air (25.4% vs. 19.3%, p&lt;0.05) and after exposure of mice to hypoxia-reoxygenation (31.7% vs. 23.0%, p&lt;0.05). In addition, resting leukocytes from S+S-Antilles mice produce 1.8-fold more H2O2 than normal mice (p&lt;0.05) as measured by Amplex Red (10-acetyl-3,7-dihydroxyphenoxazine) fluorescence. These leukocyte oxidants are especially toxic in the presence of excess redox active iron. Histopathology of the lungs and livers of 10 week old S+S-Antilles and BERK sickle mice showed red blood cell (RBC) congestion compared to normal. In addition, the sickle livers had multiple areas of infarction and inflammatory leukocyte infiltration. The heme contents of S+S-Antilles sickle lungs and livers were increased by 37- and 4.9-fold, respectively, compared to normals (p&lt;0.05 for both organs). Furthermore, there was significantly more chelatable iron that is potentially redox active as measured by Ferene-S in sickle lungs (21.0-fold, p&lt;0.05) and livers (2.4-fold, p&lt;0.05) compared to normals. Thus, these data demonstrate there is an explosive pro-oxidative environment in sickle mice. These excess oxidants lead to NF-kB activation, VCAM-1 and ICAM-1 expression, and increased oxidative injury, as seen histopathologically by nitro-tyrosine and dihydroethidium staining in organs. Hypoxia-reoxygenation, which induces RBC sickling and enhances ROS production in sickle mice, causes an increase in leukocyte rolling (4.4-fold, S+S-Antilles vs. normal, p&lt;0.05) and adhesion (6.5-fold, p&lt;0.05). Hypoxia-reoxygenation induces transient vaso-occlusion in 12% and 24% of the subcutaneous venules of S+S-Antilles and BERK mice respectively. No vessels become static in normal mice (p&lt;0.05 sickle vs. normal). Hypoxia-reoxygenation-induced vaso-occlusion can be inhibited by antibodies to P-selectin, VCAM-1 or ICAM-1. Furthermore, scavenging ROS with the SOD and catalase mimetic, polynitroxyl albumin or the iron chelator Trimidox, inhibited hypoxia-reoxygenation-induced vaso-occlusion (p&lt;0.05). We conclude that oxidative stress derived from activated leukocytes and excess redox active iron plays a critical role in promoting vaso-occlusion and organ injury in SCD. We speculate that iron chelators, leukocyte adhesion molecule blockade and anti-oxidants will modulate vaso-occlusion in patients with SCD.

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