Plasma iron status and lipid peroxidation following thrombolytic therapy for acute myocardial infarction

Superoxide is capable of mobilizing iron from ferritin and the released

Iron, Dopamine, and α-Synuclein Interactions in at-Risk Dopaminergic Neurons in Parkinson’s Disease

 becomes toxic in dopaminergic neurons by (1) reacting with 

 & Junxia Xie jxiaxie@163.com; jxiaxie@public.qd.sd.cn

Monoamine oxidase inhibitors, and iron chelators in depressive illness and neurodegenerative diseases

 and lead to Fenton reaction and production of the most reactive radical, namely hydroxyl radical.

Oxidative damage to food and human serum proteins: Radical-mediated oxidation vs. glyco-oxidation.

 for the production of glycosylative and oxidative species, respectively.

Role of iron in lung injury-induced by hyperoxia.

 can damage tissues by catalyzing the conversion of 

 to free-radical ions that attack lipids, proteins and DNA.

Iron-activated iron uptake: A positive feedback loop mediated by iron regulatory protein 1

 activates IRP1 and that this activation mediates a potentially harmful increase in 

Therapeutic benefits of antioxidants during sepsis: is protection against oxidant-mediated tissue damage only half the story?

Thus, conditions favoring the formation of

 are potentially catastrophic to the host.

Role of Free Radicals in the Neurodegenerative Diseases

 is a powerful promoter of free radical damage, able to catalyse generation of highly reactive hydroxyl, alkoxyl and peroxyl radicals from 

1-Hydroxyethyl radical formation during NADPH- and NADH-dependent oxidation of ethanol by human liver microsomes.

HER formation by human liver microsomes seems to be catalyzed by an oxidant derived from the interaction of

, and a close association exists between HER formation and superoxide production.

A site-specific mechanism for free radical induced biological damage: the essential role of redox-active transition metals.

 are soluble enough, and the rate constants of their reduced forms with 

 are sufficiently high to suggest that they might be important mediators of free radical toxicity.

Ferritin and haemosiderin in free radical generation, lipid peroxidation and protein damage.

 promotes both hydroxyl radical formation in the presence of 

The role of hydrogen peroxide and singlet oxygen in the photodegradation of melanin.

 strongly accelerated melanin degradation induced by 

, it had very little influence on the rate of photodegradation of melanin.

Combined Fenton and starvation therapies using hemoglobin and glucose oxidase.

 ions from the heme groups of hemoglobin also release in the presence of both endogenous and produced 

Deferoxamine: potential novel topical therapeutic for chronic wounds

 (from activated neutrophils) generates ferric ion (Fe) and reactive oxygen species (ROS), the prolonged production of which results in a chronically inflamed environment.

MOF-Mediated Destruction of Cancer Using the Cell's Own Hydrogen Peroxide.

 present on the rMOF-FA and released into solution can react with high levels of 

 found specifically in cancer cells to increase the hydroxyl radical concentration.

[Comparation of Toxic Effect of Silicious Mineral Dusts on Lung Epithelial A549 Cells].

 exhibited a linear correlation with the 

 content, which meant that iron in the mineral dusts played an important role in the generation of reactive radical.

Intracellular labile iron determines H2O2-induced apoptotic signaling via sustained activation of ASK1/JNK-p38 axis.

 induced spatiotemporal changes in intracellular labile 

, at least in part, by triggering the destabilization of lysosomal compartments, promoting a concomitant early response in proteins of iron homeostasis.

Iron stimulates plasma-activated medium-induced A549 cell injury

 in PAM and/or •OH generated in the presence of 

 disturbed the mitochondrial-nuclear network in cancer cells.

In Situ OH Generation from O2 − and H2O2 Plays a Critical Role in Plasma-Induced Cell Death

 (H2O2) were the two major species present in plasma, but their respective concentrations were not sufficient to cause cell death when used in isolation; however, in the presence of 

, both species enhanced the cell death-inducing effects of plasma.

Role of labile iron in the toxicity of pharmacological ascorbate.

 in cell culture media contributes significantly to the rate of 

Extracellular iron diminishes anticancer effects of vitamin C: An in vitro study

A detailed examination of mechanisms showed that

 at physiological concentrations promotes both production and decomposition of 

Increased endogenous DNA oxidation correlates to increased iron levels in melanocytes relative to keratinocytes.

To account for the increased oxidative DNA and lower GSH and H2O2 levels that we observe, we propose that

 may contribute to higher levels of oxidation by reacting with 

 through a Fenton reaction leading to the generation of DNA-reactive hydroxyl radicals.

Iron and genome stability: an update.

 is an extremely reactive transition metal that can interact with 

 to generate hydroxyl radicals that form the 8-hydroxy-guanine adduct, cause point mutations as well as DNA single and double strand breaks.

Importance of iron chelation in free radical-induced oxidative stress and human disease.

 linked with the catalytic decomposition of 

 (Fenton reaction) leading to the formation of reactive oxygen species (ROS) causing damage to biomolecules, including lipids, proteins and DNA.

The non‐ionic surfactant poloxamer P188 does not prevent blood‐induced cartilage damage

 from damaged and phagocytosed red blood cells in the vicinity of chondrocytes, leading to the formation of radicals that induce cell death, as was shown among others by Transferase Biotin-dUTP Nick End Labeling (TUNEL) staining [3].

Bifunctional drug derivatives of MAO-B inhibitor rasagiline and iron chelator VK-28 as a more effective approach to treatment of brain ageing and ageing neurodegenerative diseases

This may result from increased glia hydrogen peroxide producing monoamine oxidase (MAO) activity that can generate of reactive hydroxyl radical formed from interaction of

Comparison of Ultrastructural Cytotoxic Effects of Carbon and Carbon/Iron Particulates on Human Monocyte-Derived Macrophages

 bound to C particles catalyzed the decomposition of 

Inhibition of apoptosis in acute promyelocytic leukemia cells leads to increases in levels of oxidized protein and LMP2 immunoproteasome.

We also show that caspase inhibition leads to increases in the levels of oxidized proteins obtained by treatments with

Role of Hydrogen Peroxide in the Aetiology of Alzheimer’s Disease

The ability for Aβ to generate H2O2, and interactions of

 and copper to generate highly toxic ROS, may provide a mechanism for the oxidative stress associated with Alzheimer’s disease.

Micromolar concentrations of hydrogen peroxide induce oxidative DNA lesions more efficiently than millimolar concentrations in mammalian cells.

Furthermore, it has been demonstrated that

 causes single-strand breaks in purified DNA in the presence of 

 and induces mitochondrial DNA damage in CHO cells with a biphasic dose-response curve.

Role of iron in alcoholic liver disease: introduction and summary of the symposium.

 can induce oxidative stress by catalyzing the conversion of superoxide and 

 to more potent oxidants such as hydroxyl radicals, which can cause tissue injury by initiating lipid peroxidation and causing oxidation of proteins and nucleic acids.

Iron metabolism, free radicals, and oxidative injury.

 is also biochemically dangerous; it can damage tissues by catalyzing the conversion of 

 to free-radical ions that attack cellular membranes, protein and DNA.

Lipid peroxidation, some extracellular antioxidants, and antioxidant enzymes in serum of patients with rheumatoid arthritis

 possibly converted to hydroxyl radical by 

 due to lower transferrin level might have led to increased serum lipid peroxidation in patients with rheumatoid arthritis.

Disorders of iron metabolism.

 can also damage tissues by catalyzing the conversion of 

 to free-radical ions that attack cellular membranes, proteins, and DNA.

Transferrin synthesized in cultured human fibroblasts is associated with tubulins and has iron binding capacity.

These results suggest that endogenous transferrin plays a role in preventing damage caused by free radicals which can be induced by the interaction of

Hydroxyl radical as a potential intracellular mediator of polymorphonuclear neutrophil apoptosis.

Oxidation of serotonin by superoxide radical: implications to neurodegenerative brain disorders.

, cogenerated by the xanthine oxidase-mediated oxidation of xanthine to uric acid, together react with trace levels of 

 that contaminate buffer constituents to give a chemically ill-defined oxo-iron species.

Cytotoxic effect of immunoconjugate composed of glucose-oxidase coupled to an anti-ganglioside (GD2) antibody on spheroids.

The cytotoxic effect of glucose-oxidase is achieved by the production of hydrogenperoxide (H2O2) and probably by the following reaction of

Myoglobin toxicity in proximal human kidney cells: roles of Fe, Ca2+, H2O2, and terminal mitochondrial electron transport.

 production (phenol red assay) suggests one potential mechanism.

Mössbauer, electron-paramagnetic-resonance and X-ray-absorption fine-structure studies of the iron environment in recombinant human tyrosine hydroxylase.

 of the native human TH to the ferric state.

In vitro cell injury by oxidized low density lipoprotein involves lipid hydroperoxide-induced formation of alkoxyl, lipid, and peroxyl radicals.

Intracellular chelation of … preloading cells with

 enhanced, toxicity, Inhibition of oxidized LDL and 7 beta-OOH chol toxicity by 2-keto-4-…, a putative alkoxyl radical scavenger and by vitamin E, probucol and diphenylphenylenediamine, putative scavengers of 

 radicals was consistent with the … radicals in the lethal sequence.

Transferrin and Iron in Normal, Alzheimer's Disease, and Parkinson's Disease Brain Regions

 to hydroxyl radical and, thus, may contribute to oxidant stress.

Biological origin of free radicals, and mechanisms of antioxidant protection.

 (Fenton chemistry) to generate hydroxyl radicals that can damage all organic molecules.

Ethambutol-Induced Ocular Toxicity Revisited

, superoxide, and hydroxyl radicals, and therefore may be one of the most potent generators of free radicals.

Hydrogen peroxide formation by cells treated with a tumor promoter.

 which entered the cells, thus decreasing its levels available for oxidation of the substrate and potentially increasing formation of .OH, known DNA-damaging species.

Bacterial iron enhances oxygen radical-mediated killing of Staphylococcus aureus by phagocytes

 loading of the bacteria markedly increased their susceptibility to killing by 

Hydrogen peroxide-mediated inhibition of T-cell response to mitogens is a result of direct action on T cells.

 and to induce lipid peroxidation, we compared the effects of hydrogen peroxide and a lipid peroxidation product, malondialdehyde, on the response of human peripheral blood mononuclear cells to T-cell mitogens.

Lactoferrin enhances hydroxyl radical production by human neutrophils, neutrophil particulate fractions, and an enzymatic generating system.

Hydroxyl radical (.OH), a particularly potent oxidant, is believed to be produced by interaction between O2- and

, according to the Haber-Weiss reactions.

The decomposition of hydrogen peroxide by hemocyanin and by its dissociation products.

 porphyrin catalase activity, it had no effect at all on the catalase activity of hemocyanin.

Disruption of a Novel Iron Transport System Reverses Oxidative Stress Phenotypes of a dpr Mutant Strain of Streptococcus mutans

Dpr accumulates during oxidative stress, protecting the cell by sequestering iron ions and thereby preventing the generation of toxic hydroxyl radicals that result from the interaction of

The Dps-like peroxide resistance protein (Dpr) is essential for H2O2 stress tolerance … preventing the generation of toxic hydroxyl radicals that result from the interaction of

 Previously, we reported that the SpxA1 and SpxA2 regulators positively regulate … cooperative nature of SpxA1 and SpxA2 regulation in Dpr production.

Peroxiredoxins are important for the regulation of hydrogen peroxide concentrations in ticks and tick cell line.

 may lead to high levels of reactive oxygen species (ROS), including 

The impairment of methylmenaquinol:fumarate reductase affects hydrogen peroxide susceptibility and accumulation in Campylobacter jejuni

 resulted in a significant decrease in total intracellular 

 in the ∆mfrA strain as compared to WT, while the addition of iron to the growth medium mitigated H2O2 susceptibility and accumulation in the mutant.

Hydrogen peroxide and extracellular signal-related kinase 1/2 pathway regulate ferritin levels in retinal pigmented and lens epithelial cells

 plays a central role in the oxidative stress caused by 

Effect of dietary iron overload in rat brain: oxidative stress, neurotransmitter level and serum metal ion in relation to neurodegenerative disorders.

 causes cell injury by reacting with superoxide anions (O2*) and 

 (H2O2) and producing hydroxyl radical (OH*) and reactive oxygen species (ROS).

Assessment of Prion Inactivation by Fenton Reaction Using Protein Misfolding Cyclic Amplification and Bioassay

 effectively reduced infectivity and the level of abnormal isoforms of the prion protein in scrapie-infected brain homogenates.

Noninvasive assessment of the relative roles of cerebral antioxidant enzymes by quantitation of pentose phosphate pathway activity

 exposure exerted a protective effect thus implicating the participation of the Fenton reaction in mediating damage caused by the oxidative insult.

Hydrogen peroxide enhanced inron-induced injury in isolated heart and ventricular cardiomyocyte in rats

 for 10 min following Fe-HQ augmented the effect of 

 with an increase in coronary LDH and CK release and myocardial MDA content, and decrease in LVDP, ± dP/dtmax and heart rate.

Iron inhibits neurotoxicity induced by trace copper and biological reductants

The potent protective activity of Fe correlated with

 inhibiting reductant-mediated Cu(I) and 

 generation in cell-free assays and reduced cellular Cu uptake by neurons.

SURFACE REACTIVITY, CYTOTOXICITY, AND TRANSFORMING POTENCY OF IRON-COVERED COMPARED TO UNTREATED REFRACTORY CERAMIC FIBERS

 increased the capability of RCFs to generate hydroxyl radicals and to catalyze the decomposition of 

[Hydrogen peroxide augments the injury effect of iron on the isolated rat heart and cardiomyocytes].

 accompanied by increases of coronary LDH, CK release and myocardial MDA content and decreases of LVDP, +/-dp/dt(max), and heart rate.

EFFECTS OF REACTIVE OXYGEN SPECIES ON INTRACELLULAR CALCIUM IN BOVINE TRACHEAL EPITHELIUM: Modulation by Nitric Oxide

These results suggest that OH … by interaction of O2- and

 may play a major role in the HX-XO induced disruption of airway epithelial Ca 2+ homeostasis, and that NO potentiates ROS-induced \[Ca2+]i response, presumably by reacting with O2- and producing OH.

Manganese: A transition metal protects nigrostriatal neurons from oxidative stress in the iron-induced animal model of Parkinsonism

 but not manganese, catalysed the Fenton reaction or the conversion of 

[The effects of deferoxamine on bovine pulmonary endothelial cell injury induced by hydrogen peroxide].

 may play an essential role in the endothelial cell injury mediated by 

Increased expression of monoamine oxidase‐B results in enhanced neurite degeneration in methamphetamine‐treated PC12 cells

 formed during this reaction can interact with free 

 to form hydroxyl radicals, which can oxidize proteins, nucleic acids, and membrane lipids, leading to terminal degeneration.

Assessment of the Role of the Glutathione and Pentose Phosphate Pathways in the Protection of Primary Cerebrocortical Cultures from Oxidative Stress

 exposure was protective and resulted in a correlation between PPP saturation and toxicity.

Metal replacement in DNA-binding zinc finger proteins and its relevance to mutagenicity and carcinogenicity through free radical generation.

 catalyze the degradation of deoxyribose and induce DNA damage.

Rapid responses to oxidative stress mediated by iron regulatory protein.

 (Fenton reaction) intimately connects oxidative stress and cellular iron metabolism.

Uteroferrin induces lipid peroxidation in endometrial and conceptus microsomal membranes and is inhibited by apotransferrin, retinol binding protein, and the uteroferrin-associated proteins.

 catalyze lipid peroxidation when combined with either 

Protein oxidation and amino acid-DNA crosslinking by nickel compounds in intact cultured cells.

Other metals capable of producing oxidative damage to BSA in the presence of

Electron spin resonance spin-trapping investigation into the effects of paraquat and desferrioxamine on hydroxyl radical generation during acute iron poisoning.

 and the partially reduced oxygen species superoxide and 

, which are generated during the metabolism of PQ2+, might be expected to stimulate .OH generation to a level above that seen in the presence of the metal ion alone.

Inhibition of the iron-catalysed formation of hydroxyl radicals by nitrosouracil derivatives: protection of mitochondrial membranes against lipid peroxidation.

 mediated Fenton reaction presumably results from inactivation of the reactivity of the metal center towards 

Intracellular myoglobin loading worsens H2O2-induced, but not hypoxia/reoxygenation-induced, in vitro proximal tubular injury.

This action may be explained by the ability of

 to catalyze the formation of the highly toxic hydroxyl radical (.OH) from 

Iron augments macrophage-mediated killing of Brucella abortus alone and in conjunction with interferon-gamma.

This is consistent with the Haber-Weiss reaction, in which

 catalyzes the generation of hydroxyl radicals from 

Simultaneous measurements of conjugated dienes and free malondialdehyde, used as a micromethod for the evaluation of lipid peroxidation in rat hepatocyte cultures.

This discrepancy could be ascribed to an increased decomposition of

Stimulation by paraquat of microsomal and cytochrome P-450-dependent oxidation of glycerol to formaldehyde.

An oxidant derived from the interaction of

 was responsible for oxidizing the glycerol, with P-450 suggested to be necessary to produce H2O2 and reduce non-haem iron.

Histamine release during intestinal ischemia-reperfusion: role of iron ions and hydrogen peroxide.

 and generate highly reactive oxidants, which in turn are responsible for H release.

Role of iron in the photosensitization by uroporphyrin.

 would catalyze the production of OH from 

 and the OH thus formed may have a significant role in the uroporphyrin photosensitivity.

Role of oxidants in ischemia/reperfusion-induced granulocyte infiltration.

 or hemoglobin did significantly increase the chemotactic activity of cat plasma.

The levels of quinone reductases, superoxide dismutase and glutathione-related enzymatic activities in diethylstilbestrol-induced carcinogenesis in the kidney of male Syrian golden hamsters.

The consequences of these decreases may be an increased steady-state concentration of superoxide anion and

Radiation-induced impairment of neuronal excitability.

, which produces hydroxyl free radicals when combined with 

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Possible Interaction: Hydrogen Peroxide and Iron, Dietary

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Hydrogen Peroxide

Iron, Dietary

Research Papers that Mention the Interaction