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bp(MESH:"Oxidative Stress")

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Entity

Name
Oxidative Stress
Namespace
mesh
Namespace Version
20180906
Namespace URL
https://raw.githubusercontent.com/pharmacome/terminology/b46b65c3da259b6e86026514dfececab7c22a11b/external/mesh-names.belns

Appears in Networks 7

Clearance systems in the brain-implications for Alzheimer disease. v1.0.1

TAU and Interaction Partners v1.2.5

TAU Interactions Section of NESTOR

Tau Modifications v1.9.5

Tau Modifications Sections of NESTOR

Oxidative stress in health and disease: The therapeutic potential of Nrf2 activation v1.0.0

Nuclear Factor Kappa-light-chain-enhancer of Activated B Cells (NF-κB) - a Friend, a Foe, or a Bystander - in the Neurodegenerative Cascade and Pathogenesis of Alzheimer's Disease v1.0.0

Significance of NF-κB as a pivotal therapeutic target in the neurodegenerative pathologies of Alzheimer's disease and multiple sclerosis v1.0.0

Heme Curation v0.0.1-dev

Mechanistic knowledge surrounding heme

In-Edges 50

a(CHEBI:"hydrogen peroxide") increases bp(MESH:"Oxidative Stress") View Subject | View Object

Primary cortical neurons exposed to the mitochondrial toxin NaN3 (0.1-3 mM) were submitted to oxidative stress with H2O2 (30-150 μM), to mimic conditions observed in neurodegenerative disorders. The effects of such treatment on a series of parameters useful in characterizing neuronal damage were investigated: (i) the basal release of glutamate, evaluated as (3)H-d-Aspartate efflux, was sharply, concentration-dependently, increased; (ii) the phosphorylation status of intracellular markers known to be involved in the neurodegenerative processes, in particular in Alzheimer disease: tau and GSK3β were increased, as well as the protein level of β-secretase (BACE1) and p35/25 evaluated by Western blotting, while (iii) the cell metabolic activity, measured with the MTT method, was reduced, in a concentration- and time-dependent manner. The latter effect, as well as tau hyperphosphorylation, was prevented both by a mixture of antioxidant drugs (100 μM ascorbic acid, 10 μM trolox, 100 μM glutathione) and by the anti-Alzheimer drug, memantine, 20 μM. PubMed:23722080

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Uberon
cerebral cortex

act(p(HGNC:GLP1R)) decreases bp(MESH:"Oxidative Stress") View Subject | View Object

In this study, we demonstrated that GLP-1RA could inhibit oxidative stress and repair mitochondrial damage in addition to decreasing tau hyperphosphorylation in PC12 cells treated with AGEs. Importantly, we first observed AGEs in the circulatory system could induce tau hyperphosphorylation after we injected AGEs (1μg/kg bodyweight) into the mice tail vein. We found GLP-1RA could promote mitochondrial biogenesis and antioxidant system via regulating peroxisome proliferator-activated receptor γ coactivator 1α (PGC-1α) signaling pathway in vivo besides down-regulating the activity of glycogen synthase kinase 3β (GSK-3β) to reverse tau hyperphosphorylation directly. PubMed:25987199

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p(HGNC:GSK3B) positiveCorrelation bp(MESH:"Oxidative Stress") View Subject | View Object

Nuclear factor erythroid-2-related factor 2 (Nrf2) is a transcription factor known to increase the level of many antioxidants, including glutathione-S transferase (GST), and is negatively regulated by the activity of GSK-3β. Our results indicated the increased nuclear localization of Nrf2 and level of GST, suggesting the increased activity of the transcription factor as a result of GSK-3β suppression, consistent with the decreased oxidative stress observed. Consistent with the improved learning and memory, and consistent with GSK-3b being a tau kinase, we observed decreased tau phosphorylation in brain of GAO-treated SAMP8 mice compared to that of RAO-treated SAMP8 mice. PubMed:24355211

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path(MESH:"Alzheimer Disease") positiveCorrelation bp(MESH:"Oxidative Stress") View Subject | View Object

A likely explanation for the increased expression of GLRX2 (glutaredoxin 2) and NQO1 (NAD(P)H dehydrogenase, quinone 1) in colon carcinoma and of GLRX (glutaredoxin), HMOX1 (heme oxygenase-1), NQO1, and SOD1 (superoxide dismutase 1) in Alzheimer is that it represents an adaptive attempt to partially compensate for the increased level of oxidative stress associated with these diseases. These antioxidant genes are also upregulated by Protandim, which would provide additional antioxidant protection beyond that achieved by the ROS-dependent induction of these enzymes in the diseased tissues. PubMed:22020111

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path(MESH:"Colorectal Neoplasms") positiveCorrelation bp(MESH:"Oxidative Stress") View Subject | View Object

A likely explanation for the increased expression of GLRX2 (glutaredoxin 2) and NQO1 (NAD(P)H dehydrogenase, quinone 1) in colon carcinoma and of GLRX (glutaredoxin), HMOX1 (heme oxygenase-1), NQO1, and SOD1 (superoxide dismutase 1) in Alzheimer is that it represents an adaptive attempt to partially compensate for the increased level of oxidative stress associated with these diseases. These antioxidant genes are also upregulated by Protandim, which would provide additional antioxidant protection beyond that achieved by the ROS-dependent induction of these enzymes in the diseased tissues. PubMed:22020111

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a(CHEBI:"amyloid-beta") association bp(MESH:"Oxidative Stress") View Subject | View Object

Amyloid-β induced apoptosis has also been ascribed to dyshomeostasis of intracellular Ca2+ and oxidative stress [106-108], two critical biochemical derangements known to activate NF-κB PubMed:28745240

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MeSH
Alzheimer Disease

a(CHEBI:"amyloid-beta") increases bp(MESH:"Oxidative Stress") View Subject | View Object

In primary neuronal cultures, Amyloid-β has been shown to elicit oxidative stress and evoke NF-κB activation PubMed:28745240

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MeSH
Alzheimer Disease

p(HGNC:SOD2) decreases bp(MESH:"Oxidative Stress") View Subject | View Object

Furthermore, Amyloid-β –induced NF-κB also results in the up-regulation of the antioxidant mitochondrial membrane enzyme – MnSOD (superoxide dismutase 2) [328] which is well known to combat oxidative stress and apoptosis PubMed:28745240

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MeSH
Alzheimer Disease

a(CHEBI:"4-hydroxynon-2-enal") positiveCorrelation bp(MESH:"Oxidative Stress") View Subject | View Object

Hepatic 4-hydroxynonenol (4-HNE), a marker of oxidative stress, was significantly lower in the liver microsomes of SSmice 24 hours after infusion of Hp or Hpx compared to vehicle-treated SS-mice (Fig 2G). PubMed:29694434

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Annotations
MeSH
Liver
MeSH
Anemia, Sickle Cell
Text Location
Results

a(CHEBI:"hydrogen peroxide") increases bp(MESH:"Oxidative Stress") View Subject | View Object

Once intercalated into cellular plasma membranes heme amplifies cellular susceptibility to oxidative-mediated injury by oxidants such as H2O2 or those derived from activated inflammatory cells (Balla et al., 1991a,b, 1993). PubMed:24904418

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Cell Ontology (CL)
erythrocyte
Text Location
Review

a(CHEBI:"iron(2+)") positiveCorrelation bp(MESH:"Oxidative Stress") View Subject | View Object

This engenders the release of iron, which can promote further the oxidation of plaque lipids through redox cycling reactions. The result of these chemical reactions is the formation of deleterious oxidized ‘gruel’ which, among other things, leads to endothelial oxidative stress and ultimately to cytotoxicity. PubMed:20378845

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Cell Ontology (CL)
endothelial cell
MeSH
Plaque, Atherosclerotic
Text Location
Discussion

a(CHEBI:"iron(2+)") positiveCorrelation bp(MESH:"Oxidative Stress") View Subject | View Object

Thus, by participating in Fenton chemistry, non-transferrin-bound iron (i.e., iron not bound to the physiological iron transport protein, transferrin) causes oxidative damage, cytotoxicity and enhanced endothelial expression of adhesion molecules, thereby enhancing thrombotic risk (Hershko, 2007). PubMed:25307023

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Cell Ontology (CL)
endothelial cell
MeSH
Plasma
MeSH
Urine
MeSH
Anemia, Hemolytic, Autoimmune
Text Location
Review

a(CHEBI:"iron(2+)") positiveCorrelation bp(MESH:"Oxidative Stress") View Subject | View Object

Extracellular hemoglobin and its degradation products, free heme and iron, are highly toxic due to oxidative stress induction and decrease in nitric oxide availability. PubMed:28088643

Appears in Networks:
Annotations
MeSH
Erythrocytes
MeSH
Anemia, Sickle Cell
Text Location
Abstract

a(CHEBI:"iron(2+)") positiveCorrelation bp(MESH:"Oxidative Stress") View Subject | View Object

Hb and its degradation products – free heme and iron - perpetuate oxidative stress, and together with decreased NO availability promote many SCD complications. PubMed:28088643

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Annotations
MeSH
Erythrocytes
MeSH
Anemia, Sickle Cell
Text Location
Introduction

a(CHEBI:glutathione) negativeCorrelation bp(MESH:"Oxidative Stress") View Subject | View Object

Reduced glutathione (GSH) was also depleted after 4 h of heme exposure, indicating that heme induces oxidative stress in exposed cells (Figure 5c). PubMed:26794659

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Cell Ontology (CL)
epithelial cell
MeSH
Kidney
Text Location
Results

a(CHEBI:heme) increases bp(MESH:"Oxidative Stress") View Subject | View Object

The large amounts of haem released upon haemolysis can overwhelm the capacity of haem scavengers and enzyme systems (i.e., HMOX1), thus causing oxidative stress (Jeney et al, 2002). PubMed:25307023

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Annotations
Cell Ontology (CL)
erythrocyte
MeSH
Plasma
MeSH
Urine
MeSH
Anemia, Hemolytic, Autoimmune
Text Location
Review

a(CHEBI:heme) positiveCorrelation bp(MESH:"Oxidative Stress") View Subject | View Object

Reduced glutathione (GSH) was also depleted after 4 h of heme exposure, indicating that heme induces oxidative stress in exposed cells (Figure 5c). PubMed:26794659

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Cell Ontology (CL)
epithelial cell
MeSH
Kidney
Text Location
Results

a(CHEBI:heme) positiveCorrelation bp(MESH:"Oxidative Stress") View Subject | View Object

These data suggest that the estimated free heme concentrations that occur in the renal tubular system during severe intravascular hemolysis are in the range of heme concentrations that could trigger oxidative stress and cell damage to the renal epithelium. PubMed:26794659

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Cell Ontology (CL)
epithelial cell
MeSH
Kidney
Text Location
Results

a(CHEBI:heme) increases bp(MESH:"Oxidative Stress") View Subject | View Object

Most studies concerning the pathophysiological roles of heme have focused on the protective effect of the heme-degrading enzyme, heme oxygenase 1 (HO-1) [25] (Box 2), and on the effect of this danger-associated molecule on cells, leading to oxidative stress, TLR4 signaling [26,27], and NLRP3 inflammasome activation [28] (Box 4). PubMed:26875449

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Review

a(CHEBI:heme) increases bp(MESH:"Oxidative Stress") View Subject | View Object

Extracellular hemoglobin and its degradation products, free heme and iron, are highly toxic due to oxidative stress induction and decrease in nitric oxide availability. PubMed:28088643

Appears in Networks:
Annotations
MeSH
Erythrocytes
MeSH
Anemia, Sickle Cell
Text Location
Abstract

a(CHEBI:heme) increases bp(MESH:"Oxidative Stress") View Subject | View Object

Hb and its degradation products – free heme and iron - perpetuate oxidative stress, and together with decreased NO availability promote many SCD complications. PubMed:28088643

Appears in Networks:
Annotations
MeSH
Erythrocytes
MeSH
Anemia, Sickle Cell
Text Location
Introduction

a(CHEBI:heme) increases bp(MESH:"Oxidative Stress") View Subject | View Object

Increased plasma concentrations of cell-free heme, the breakdown product of 390 hemoglobin, promote activation and inflammation of endothelial cells and enhance 391 oxidative stress and vascular permeability (22). PubMed:28314763

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Cell Ontology (CL)
endothelial cell
MeSH
Arteries
MeSH
Diabetes Mellitus
Text Location
Introduction

a(CHEBI:heme) increases bp(MESH:"Oxidative Stress") View Subject | View Object

In agreement with data on pro-oxidant effects of heme in neonatal mouse CMs (Figure 1D-F), oxidative stress was significantly increased in adult rat CMs exposed to free heme (see Figure 1 in [37]). PubMed:28400318

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Cell Ontology (CL)
regular cardiac myocyte
Text Location
Results

a(CHEBI:heme) positiveCorrelation bp(MESH:"Oxidative Stress") View Subject | View Object

Free hemin is a cytotoxic molecule that mediates oxidative stress, endothelial activation, and inflammation, and it is implicated in malaria pathogenesis [40] and AKI, among others [41]. PubMed:28716864

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Cell Ontology (CL)
neutrophil
MeSH
Serum
MeSH
Malaria
Text Location
Discussion

a(CHEBI:heme) positiveCorrelation bp(MESH:"Oxidative Stress") View Subject | View Object

During hemolysis, hemoglobin and heme released from red blood cells promote oxidative stress, inflammation and thrombosis. PubMed:29694434

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Introduction

a(CHEBI:heme) increases bp(MESH:"Oxidative Stress") View Subject | View Object

Cell-free hemoglobin and its prosthetic group heme can contribute to organ dysfunction and death [1–4, 9–12]; the pathological mechanisms include nitric oxide consumption, vasoconstriction, oxidative injury to lipid membranes, activation of the transcription factor NF-κB, endothelial injury as well as iron-driven oxidative inhibition of glucose metabolism[10–14]. PubMed:29956069

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Review

a(CHEBI:malonaldehyde) positiveCorrelation bp(MESH:"Oxidative Stress") View Subject | View Object

Malondialdehyde (MDA) represents evidence of systemic oxidative stress and inflammation [31], and is commonly used to estimate the level of lipid peroxidation. PubMed:30324533

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MeSH
Hematoma
Text Location
Results

a(HM:"nitrite oxidation") positiveCorrelation bp(MESH:"Oxidative Stress") View Subject | View Object

In other words, the faster rate of d7 nitrite oxidation predicted greater extents of oxidative damage incurred by the RBCs during storage. PubMed:26202471

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Discussion

a(HM:"stored erythrocytes") positiveCorrelation bp(MESH:"Oxidative Stress") View Subject | View Object

Storage is known to result in increased hemolysis which in turn results in loss of NO-signaling, oxidative stress and inflammation post-transfusion. PubMed:26202471

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Discussion

a(MESH:"Erythrocytes, Abnormal") positiveCorrelation bp(MESH:"Oxidative Stress") View Subject | View Object

Under conditions of apoptosis or RBC damage, such as high shear rates, inflammation, or oxidative stress, RBCs can lose membrane asymmetry and expose phosphatidylserine [43]. PubMed:28458720

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Annotations
MeSH
Veins
MeSH
Anemia, Sickle Cell
MeSH
beta-Thalassemia
Text Location
Review

a(MESH:"Reactive Oxygen Species") increases bp(MESH:"Oxidative Stress") View Subject | View Object

As a part of the inflammatory response after injury, oxidative stress due to formation of reactive oxygen species (ROS) is involved both in direct damage of cartilage components and as integral factors in cell signaling leading to cartilage degradation (Henrotin et al., 2003). PubMed:30505280

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MeSH
Knee
MeSH
Osteoarthritis, Knee
Text Location
Introduction

bp(GO:"protein oxidation") positiveCorrelation bp(MESH:"Oxidative Stress") View Subject | View Object

Oxidation of proteins result in stable carbonyl groups on amino acid side chains, and protein carbonyl content is one of the most widely used marker of protein oxidation and a general indicator of oxidative stress (Dalle-Donne et al., 2003). PubMed:30505280

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MeSH
Knee
MeSH
Osteoarthritis, Knee
Text Location
Introduction

bp(MESH:"Erythrocyte Deformability") negativeCorrelation bp(MESH:"Oxidative Stress") View Subject | View Object

It has been shown that RBC oxidative stress that damages the membrane reduces the deformability and flexibility of cells. PubMed:23215741

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Cell Ontology (CL)
erythrocyte
Text Location
Results

p(HGNC:HBB) increases bp(MESH:"Oxidative Stress") View Subject | View Object

Depending on the scale, rate, and site of hemolysis, the primary adverse effects triggered by free Hb are vascular dysfunction, oxidative tissue damage, and altered inflammatory response [1], PubMed:26475040

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MeSH
Anemia, Sickle Cell
Text Location
Abstract

p(HGNC:HBB) increases bp(MESH:"Oxidative Stress") View Subject | View Object

Extracellular hemoglobin and its degradation products, free heme and iron, are highly toxic due to oxidative stress induction and decrease in nitric oxide availability. PubMed:28088643

Appears in Networks:
Annotations
MeSH
Erythrocytes
MeSH
Anemia, Sickle Cell
Text Location
Abstract

p(HGNC:HBB) positiveCorrelation bp(MESH:"Oxidative Stress") View Subject | View Object

During hemolysis, hemoglobin and heme released from red blood cells promote oxidative stress, inflammation and thrombosis. PubMed:29694434

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Text Location
Introduction

p(HGNC:HBB) positiveCorrelation bp(MESH:"Oxidative Stress") View Subject | View Object

In addition to inflammation, cell-free hemoglobin (Hb) released via hemolysis is a potent inducer of oxidative stress. PubMed:30505280

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MeSH
Knee
MeSH
Osteoarthritis, Knee
Text Location
Introduction

complex(a(CHEBI:heme), p(INTERPRO:"NEAT domain")) decreases bp(MESH:"Oxidative Stress") View Subject | View Object

This ability of NEAT can decrease the level of NO scavenging and oxidative stress in SCD. PubMed:28088643

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MeSH
Liver
MeSH
Macrophages
MeSH
Anemia, Sickle Cell
Text Location
Discussion

p(MGI:Hpx) decreases bp(MESH:"Oxidative Stress") View Subject | View Object

Staining of CMs with a fluorescent probe for specific detection of mitochondrial superoxide (Mito-sox) confirmed lower oxidative stress in cells exposed to Hx-heme than in those exposed to albumin-heme or heme alone (Figure 1E). PubMed:28400318

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Cell Ontology (CL)
regular cardiac myocyte
Text Location
Results

p(MGI:Hpx) decreases bp(MESH:"Oxidative Stress") View Subject | View Object

Both ROS and lipid peroxidation were increased in the heart of Hx-/- mice compared to that of wild-type animals (Figure 2C, D). PubMed:28400318

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Cell Ontology (CL)
regular cardiac myocyte
Text Location
Results

p(MGI:Prdx2) negativeCorrelation bp(MESH:"Oxidative Stress") View Subject | View Object

PRDX2 deficiency, thus, causes cells to undergo more oxidative stress during in vitro aging, even in the presence of catalase. PubMed:23215741

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Cell Ontology (CL)
erythrocyte
Text Location
Results

p(MGI:Prdx2) negativeCorrelation bp(MESH:"Oxidative Stress") View Subject | View Object

PRDX2, which is able to react with low levels of H2O2 even at reduced glutathione levels, may therefore play a role in limiting the increased formation of heme degradation products in older cells. PubMed:23215741

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Cell Ontology (CL)
erythrocyte
Text Location
Discussion

p(MGI:Prdx2) negativeCorrelation bp(MESH:"Oxidative Stress") View Subject | View Object

Peroxiredoxin-2 (Prx-2) has emerged as the critical antioxidant protecting RBCs from H2O2 produced endogenously (by Hb autoxidation and subsequent superoxide dismutation) and exogenously (e.g., from activated neutrophils) at low (physiologic) concentrations (11, 32, 38, 40, 43, 45) and, therefore, may limit oxidative injury to other cells/tissues in the vasculature (6, 57). PubMed:25264713

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Cell Ontology (CL)
erythrocyte
Text Location
Introduction

p(MGI:Prdx2) decreases bp(MESH:"Oxidative Stress") View Subject | View Object

This is consistent with increased Prx-2 oxidation and a role for this enzyme in protecting RBC membrane constituents from storage-dependent oxidative stress (49, 50). PubMed:25264713

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Cell Ontology (CL)
erythrocyte
Text Location
Discussion

p(MGI:Prdx2) decreases bp(MESH:"Oxidative Stress") View Subject | View Object

The potential significance of this finding is underscored by the fact that Prx-2 is considered the primary antioxidant system to negate H2O2-mediated oxidative damage in the RBC (41). PubMed:25264713

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Cell Ontology (CL)
erythrocyte
Text Location
Discussion

p(HGNC:AMBP) decreases bp(MESH:"Oxidative Stress") View Subject | View Object

Another protein that in the last decade has been shown to play a central role as a protective protein against oxidative stress is a1-microglobulin (A1M) (Åkerström and Gram, 2014). PubMed:30505280

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MeSH
Knee
MeSH
Osteoarthritis, Knee
Text Location
Introduction

p(HGNC:EIF2AK1) negativeCorrelation bp(MESH:"Oxidative Stress") View Subject | View Object

In other words, Hri is necessary for erythroid differentiation and survival under oxidative stress. PubMed:25411909

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Introduction

p(HGNC:FTH1) decreases bp(MESH:"Oxidative Stress") View Subject | View Object

Cells deficient on FtH are more susceptible to oxidative damage, while increased amounts of FtH protects cells from death induced by challenges such as Fe, tumor necrosis factor (TNF), heme, heme plus TNF, or oxidized low-density lipoprotein (LDL; Juckett et al., 1995; Pham et al., 2004; Gozzelino et al., 2012). PubMed:24904418

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Review

p(HGNC:PRDX2) negativeCorrelation bp(MESH:"Oxidative Stress") View Subject | View Object

While it is clear that PRDX2 plays an important role in protecting RBCs from oxidative stress, the relative importance of PRDX2 in scavenging H2O2 in RBC has not been fully elucidated. PubMed:23215741

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Introduction

p(MGI:Hmox1) decreases bp(MESH:"Oxidative Stress") View Subject | View Object

A recent study indicated that expression of HO-1 targeted to mitochondria attenuated oxidative stress (43). PubMed:26974230

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Cell Ontology (CL)
endothelial cell
MeSH
Mitochondria
Text Location
Discussion

Out-Edges 44

bp(MESH:"Oxidative Stress") increases path(MESH:Aging) View Subject | View Object

These findings are in line with evidence suggesting that increased oxi- dative stress157 and loss of vascular integrity contribute to ageing158 and AD,159 as demonstrated by accelerated breakdown of the BBB and the neurovascular unit. PubMed:26195256

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MeSH
Hippocampus
MeSH
Temporal Lobe

bp(MESH:"Oxidative Stress") increases tloc(p(HGNC:MAPT), fromLoc(GO:cytoplasm), toLoc(GO:nucleus)) View Subject | View Object

In this work, we demonstrate that acute oxidative stress and mild heat stress (HS) induce the accumulation of dephosphorylated Tau in neuronal nuclei. Using chromatin immunoprecipitation assays, we demonstrate that the capacity of endogenous Tau to interact with neuronal DNA increased following HS. Comet assays performed on both wildtype and Tau-deficient neuronal cultures showed that Tau fully protected neuronal genomic DNA against HS-induced damage. Interestingly, HS-induced DNA damage observed in Tau-deficient cells was completely rescued after the overexpression of human Tau targeted to the nucleus. PubMed:21131359

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bp(MESH:"Oxidative Stress") increases act(p(FPLX:JNK)) View Subject | View Object

Only middle-aged Tet-mev-1 mice showed JNK/MARK activation and Ca2+ overload, particularly in astrocytes with decreased hippocampal GFAP and S100ß, but without pathological features such as apoptosis, amyloidosis, and lactic acidosis in neurons and astrocytes. This led to decreasing levels of glial fibrillary acidic protein and S100β in the hippocampal area. PubMed:27623715

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Uberon
hippocampal formation
Cell Ontology (CL)
astrocyte

bp(MESH:"Oxidative Stress") increases a(CHEBI:"calcium(2+)") View Subject | View Object

Only middle-aged Tet-mev-1 mice showed JNK/MARK activation and Ca2+ overload, particularly in astrocytes with decreased hippocampal GFAP and S100ß, but without pathological features such as apoptosis, amyloidosis, and lactic acidosis in neurons and astrocytes. This led to decreasing levels of glial fibrillary acidic protein and S100β in the hippocampal area. PubMed:27623715

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Uberon
hippocampal formation
Cell Ontology (CL)
astrocyte

bp(MESH:"Oxidative Stress") decreases p(HGNC:S100B) View Subject | View Object

Only middle-aged Tet-mev-1 mice showed JNK/MARK activation and Ca2+ overload, particularly in astrocytes with decreased hippocampal GFAP and S100ß, but without pathological features such as apoptosis, amyloidosis, and lactic acidosis in neurons and astrocytes. This led to decreasing levels of glial fibrillary acidic protein and S100β in the hippocampal area. PubMed:27623715

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Uberon
hippocampal formation
Cell Ontology (CL)
astrocyte

bp(MESH:"Oxidative Stress") causesNoChange bp(GO:"apoptotic process") View Subject | View Object

Only middle-aged Tet-mev-1 mice showed JNK/MARK activation and Ca2+ overload, particularly in astrocytes with decreased hippocampal GFAP and S100ß, but without pathological features such as apoptosis, amyloidosis, and lactic acidosis in neurons and astrocytes. This led to decreasing levels of glial fibrillary acidic protein and S100β in the hippocampal area. PubMed:27623715

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Uberon
hippocampal formation
Cell Ontology (CL)
astrocyte
Cell Ontology (CL)
neuron

bp(MESH:"Oxidative Stress") causesNoChange path(MESH:"Acidosis, Lactic") View Subject | View Object

Only middle-aged Tet-mev-1 mice showed JNK/MARK activation and Ca2+ overload, particularly in astrocytes with decreased hippocampal GFAP and S100ß, but without pathological features such as apoptosis, amyloidosis, and lactic acidosis in neurons and astrocytes. This led to decreasing levels of glial fibrillary acidic protein and S100β in the hippocampal area. PubMed:27623715

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Annotations
Uberon
hippocampal formation
Cell Ontology (CL)
astrocyte
Cell Ontology (CL)
neuron

bp(MESH:"Oxidative Stress") causesNoChange bp(GO:"amyloid fibril formation") View Subject | View Object

Only middle-aged Tet-mev-1 mice showed JNK/MARK activation and Ca2+ overload, particularly in astrocytes with decreased hippocampal GFAP and S100ß, but without pathological features such as apoptosis, amyloidosis, and lactic acidosis in neurons and astrocytes. This led to decreasing levels of glial fibrillary acidic protein and S100β in the hippocampal area. PubMed:27623715

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Annotations
Uberon
hippocampal formation
Cell Ontology (CL)
astrocyte
Cell Ontology (CL)
neuron

bp(MESH:"Oxidative Stress") decreases a(GO:mitochondrion) View Subject | View Object

Primary cortical neurons exposed to the mitochondrial toxin NaN3 (0.1-3 mM) were submitted to oxidative stress with H2O2 (30-150 μM), to mimic conditions observed in neurodegenerative disorders. The effects of such treatment on a series of parameters useful in characterizing neuronal damage were investigated: (i) the basal release of glutamate, evaluated as (3)H-d-Aspartate efflux, was sharply, concentration-dependently, increased; (ii) the phosphorylation status of intracellular markers known to be involved in the neurodegenerative processes, in particular in Alzheimer disease: tau and GSK3β were increased, as well as the protein level of β-secretase (BACE1) and p35/25 evaluated by Western blotting, while (iii) the cell metabolic activity, measured with the MTT method, was reduced, in a concentration- and time-dependent manner. The latter effect, as well as tau hyperphosphorylation, was prevented both by a mixture of antioxidant drugs (100 μM ascorbic acid, 10 μM trolox, 100 μM glutathione) and by the anti-Alzheimer drug, memantine, 20 μM. PubMed:23722080

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Uberon
cerebral cortex

bp(MESH:"Oxidative Stress") positiveCorrelation p(HGNC:GSK3B) View Subject | View Object

Nuclear factor erythroid-2-related factor 2 (Nrf2) is a transcription factor known to increase the level of many antioxidants, including glutathione-S transferase (GST), and is negatively regulated by the activity of GSK-3β. Our results indicated the increased nuclear localization of Nrf2 and level of GST, suggesting the increased activity of the transcription factor as a result of GSK-3β suppression, consistent with the decreased oxidative stress observed. Consistent with the improved learning and memory, and consistent with GSK-3b being a tau kinase, we observed decreased tau phosphorylation in brain of GAO-treated SAMP8 mice compared to that of RAO-treated SAMP8 mice. PubMed:24355211

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bp(MESH:"Oxidative Stress") increases p(HGNC:MAPT, pmod(HBP:hyperphosphorylation)) View Subject | View Object

>8 phosphates per tau molecules (vs 2 in adult healthy brain); can also be increased during development, hibernation and temperature, heat and oxydative stress These phosphorylated states are detected by specific antibodies and are targets of proline-directed kinases (SP motifs), non-proline kinases (KXGS motif) Weakens tau-MT interaction especially S261 in R1 and S214 in proline-rich domain PubMed:8226987

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bp(MESH:"Oxidative Stress") increases a(HBP:"paired helical filaments") View Subject | View Object

Though whole tau assembled poorly, constructs containing three internal repeats (corresponding to the fetal tau isoform) formed PHFs reproducibly. This ability depended on intermolecular disulfide bridges formed by the single Cys-322. Blocking the SH group, mutating Cys for Ala, or keeping T in a reducing environment all inhibited assembly. On the other hand, Cys-322 can be oxidized, and this leads to PHF assembly (ref. 11; this report). In vitro this is achieved most easily by using constructs of the 'fetal' isoform of T (htau23) that has only three repeats. Conversely, reducing agents or the second repeat or T can be viewed as 'antidotes' against PHF assembly.The synthetic PHFs bound the dye thioflavin S used in Alzheimer disease diagnostics. PubMed:7667312

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bp(MESH:"Oxidative Stress") positiveCorrelation path(MESH:"Colorectal Neoplasms") View Subject | View Object

A likely explanation for the increased expression of GLRX2 (glutaredoxin 2) and NQO1 (NAD(P)H dehydrogenase, quinone 1) in colon carcinoma and of GLRX (glutaredoxin), HMOX1 (heme oxygenase-1), NQO1, and SOD1 (superoxide dismutase 1) in Alzheimer is that it represents an adaptive attempt to partially compensate for the increased level of oxidative stress associated with these diseases. These antioxidant genes are also upregulated by Protandim, which would provide additional antioxidant protection beyond that achieved by the ROS-dependent induction of these enzymes in the diseased tissues. PubMed:22020111

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bp(MESH:"Oxidative Stress") positiveCorrelation path(MESH:"Alzheimer Disease") View Subject | View Object

A likely explanation for the increased expression of GLRX2 (glutaredoxin 2) and NQO1 (NAD(P)H dehydrogenase, quinone 1) in colon carcinoma and of GLRX (glutaredoxin), HMOX1 (heme oxygenase-1), NQO1, and SOD1 (superoxide dismutase 1) in Alzheimer is that it represents an adaptive attempt to partially compensate for the increased level of oxidative stress associated with these diseases. These antioxidant genes are also upregulated by Protandim, which would provide additional antioxidant protection beyond that achieved by the ROS-dependent induction of these enzymes in the diseased tissues. PubMed:22020111

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bp(MESH:"Oxidative Stress") association a(CHEBI:"amyloid-beta") View Subject | View Object

Amyloid-β induced apoptosis has also been ascribed to dyshomeostasis of intracellular Ca2+ and oxidative stress [106-108], two critical biochemical derangements known to activate NF-κB PubMed:28745240

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MeSH
Alzheimer Disease

bp(MESH:"Oxidative Stress") increases act(complex(GO:"NF-kappaB complex")) View Subject | View Object

Amyloid-β induced apoptosis has also been ascribed to dyshomeostasis of intracellular Ca2+ and oxidative stress [106-108], two critical biochemical derangements known to activate NF-κB PubMed:28745240

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MeSH
Alzheimer Disease

bp(MESH:"Oxidative Stress") increases act(complex(GO:"NF-kappaB complex")) View Subject | View Object

NF-κB acts as a sensor of oxidative stress and it is well established that oxidative stress results in the activation of NF-κB PubMed:28745240

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MeSH
Alzheimer Disease

bp(MESH:"Oxidative Stress") increases act(complex(GO:"NF-kappaB complex")) View Subject | View Object

In primary neuronal cultures, Amyloid-β has been shown to elicit oxidative stress and evoke NF-κB activation PubMed:28745240

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MeSH
Alzheimer Disease

bp(MESH:"Oxidative Stress") increases bp(GO:"apoptotic process") View Subject | View Object

NF-κB activation also protects hippocampal neurons from oxidative stress-induced apoptosis by inducing manganese superoxide dismutase (MnSOD) expression and mitigating peroxynitrite-induced protein nitration PubMed:28745240

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MeSH
Hippocampus
MeSH
Alzheimer Disease

bp(MESH:"Oxidative Stress") increases bp(GO:"apoptotic process") View Subject | View Object

In primary neuronal cells, exposure to Aβ25-35 peptide increase NF-κB mediated transactivation of manganese superoxide dismutase (Mn-SOD), suppress peroxinitrite production and inhibit membrane depolarization, thereby preventing apoptosis induced by oxidative stress PubMed:25652642

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MeSH
Neurons
MeSH
Alzheimer Disease

bp(MESH:"Oxidative Stress") positiveCorrelation a(CHEBI:"iron(2+)") View Subject | View Object

This engenders the release of iron, which can promote further the oxidation of plaque lipids through redox cycling reactions. The result of these chemical reactions is the formation of deleterious oxidized ‘gruel’ which, among other things, leads to endothelial oxidative stress and ultimately to cytotoxicity. PubMed:20378845

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Cell Ontology (CL)
endothelial cell
MeSH
Plaque, Atherosclerotic
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Discussion

bp(MESH:"Oxidative Stress") positiveCorrelation a(CHEBI:"iron(2+)") View Subject | View Object

Thus, by participating in Fenton chemistry, non-transferrin-bound iron (i.e., iron not bound to the physiological iron transport protein, transferrin) causes oxidative damage, cytotoxicity and enhanced endothelial expression of adhesion molecules, thereby enhancing thrombotic risk (Hershko, 2007). PubMed:25307023

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Cell Ontology (CL)
endothelial cell
MeSH
Plasma
MeSH
Urine
MeSH
Anemia, Hemolytic, Autoimmune
Text Location
Review

bp(MESH:"Oxidative Stress") positiveCorrelation a(CHEBI:"iron(2+)") View Subject | View Object

Extracellular hemoglobin and its degradation products, free heme and iron, are highly toxic due to oxidative stress induction and decrease in nitric oxide availability. PubMed:28088643

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Erythrocytes
MeSH
Anemia, Sickle Cell
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Abstract

bp(MESH:"Oxidative Stress") positiveCorrelation a(CHEBI:"iron(2+)") View Subject | View Object

Hb and its degradation products – free heme and iron - perpetuate oxidative stress, and together with decreased NO availability promote many SCD complications. PubMed:28088643

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Erythrocytes
MeSH
Anemia, Sickle Cell
Text Location
Introduction

bp(MESH:"Oxidative Stress") negativeCorrelation p(HGNC:PRDX2) View Subject | View Object

While it is clear that PRDX2 plays an important role in protecting RBCs from oxidative stress, the relative importance of PRDX2 in scavenging H2O2 in RBC has not been fully elucidated. PubMed:23215741

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bp(MESH:"Oxidative Stress") negativeCorrelation bp(MESH:"Erythrocyte Deformability") View Subject | View Object

It has been shown that RBC oxidative stress that damages the membrane reduces the deformability and flexibility of cells. PubMed:23215741

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Cell Ontology (CL)
erythrocyte
Text Location
Results

bp(MESH:"Oxidative Stress") negativeCorrelation p(MGI:Prdx2) View Subject | View Object

PRDX2 deficiency, thus, causes cells to undergo more oxidative stress during in vitro aging, even in the presence of catalase. PubMed:23215741

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Cell Ontology (CL)
erythrocyte
Text Location
Results

bp(MESH:"Oxidative Stress") negativeCorrelation p(MGI:Prdx2) View Subject | View Object

PRDX2, which is able to react with low levels of H2O2 even at reduced glutathione levels, may therefore play a role in limiting the increased formation of heme degradation products in older cells. PubMed:23215741

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Cell Ontology (CL)
erythrocyte
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Discussion

bp(MESH:"Oxidative Stress") negativeCorrelation p(MGI:Prdx2) View Subject | View Object

Peroxiredoxin-2 (Prx-2) has emerged as the critical antioxidant protecting RBCs from H2O2 produced endogenously (by Hb autoxidation and subsequent superoxide dismutation) and exogenously (e.g., from activated neutrophils) at low (physiologic) concentrations (11, 32, 38, 40, 43, 45) and, therefore, may limit oxidative injury to other cells/tissues in the vasculature (6, 57). PubMed:25264713

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Cell Ontology (CL)
erythrocyte
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Introduction

bp(MESH:"Oxidative Stress") negativeCorrelation p(HGNC:EIF2AK1) View Subject | View Object

In other words, Hri is necessary for erythroid differentiation and survival under oxidative stress. PubMed:25411909

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bp(MESH:"Oxidative Stress") positiveCorrelation a(HM:"stored erythrocytes") View Subject | View Object

Storage is known to result in increased hemolysis which in turn results in loss of NO-signaling, oxidative stress and inflammation post-transfusion. PubMed:26202471

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Discussion

bp(MESH:"Oxidative Stress") positiveCorrelation a(HM:"nitrite oxidation") View Subject | View Object

In other words, the faster rate of d7 nitrite oxidation predicted greater extents of oxidative damage incurred by the RBCs during storage. PubMed:26202471

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Discussion

bp(MESH:"Oxidative Stress") negativeCorrelation a(CHEBI:glutathione) View Subject | View Object

Reduced glutathione (GSH) was also depleted after 4 h of heme exposure, indicating that heme induces oxidative stress in exposed cells (Figure 5c). PubMed:26794659

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Cell Ontology (CL)
epithelial cell
MeSH
Kidney
Text Location
Results

bp(MESH:"Oxidative Stress") positiveCorrelation a(CHEBI:heme) View Subject | View Object

Reduced glutathione (GSH) was also depleted after 4 h of heme exposure, indicating that heme induces oxidative stress in exposed cells (Figure 5c). PubMed:26794659

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Cell Ontology (CL)
epithelial cell
MeSH
Kidney
Text Location
Results

bp(MESH:"Oxidative Stress") positiveCorrelation a(CHEBI:heme) View Subject | View Object

These data suggest that the estimated free heme concentrations that occur in the renal tubular system during severe intravascular hemolysis are in the range of heme concentrations that could trigger oxidative stress and cell damage to the renal epithelium. PubMed:26794659

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Cell Ontology (CL)
epithelial cell
MeSH
Kidney
Text Location
Results

bp(MESH:"Oxidative Stress") positiveCorrelation a(CHEBI:heme) View Subject | View Object

Free hemin is a cytotoxic molecule that mediates oxidative stress, endothelial activation, and inflammation, and it is implicated in malaria pathogenesis [40] and AKI, among others [41]. PubMed:28716864

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Cell Ontology (CL)
neutrophil
MeSH
Serum
MeSH
Malaria
Text Location
Discussion

bp(MESH:"Oxidative Stress") positiveCorrelation a(CHEBI:heme) View Subject | View Object

During hemolysis, hemoglobin and heme released from red blood cells promote oxidative stress, inflammation and thrombosis. PubMed:29694434

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Introduction

bp(MESH:"Oxidative Stress") positiveCorrelation a(MESH:"Erythrocytes, Abnormal") View Subject | View Object

Under conditions of apoptosis or RBC damage, such as high shear rates, inflammation, or oxidative stress, RBCs can lose membrane asymmetry and expose phosphatidylserine [43]. PubMed:28458720

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MeSH
Veins
MeSH
Anemia, Sickle Cell
MeSH
beta-Thalassemia
Text Location
Review

bp(MESH:"Oxidative Stress") positiveCorrelation p(HGNC:HBB) View Subject | View Object

During hemolysis, hemoglobin and heme released from red blood cells promote oxidative stress, inflammation and thrombosis. PubMed:29694434

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bp(MESH:"Oxidative Stress") positiveCorrelation p(HGNC:HBB) View Subject | View Object

In addition to inflammation, cell-free hemoglobin (Hb) released via hemolysis is a potent inducer of oxidative stress. PubMed:30505280

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Knee
MeSH
Osteoarthritis, Knee
Text Location
Introduction

bp(MESH:"Oxidative Stress") positiveCorrelation a(CHEBI:"4-hydroxynon-2-enal") View Subject | View Object

Hepatic 4-hydroxynonenol (4-HNE), a marker of oxidative stress, was significantly lower in the liver microsomes of SSmice 24 hours after infusion of Hp or Hpx compared to vehicle-treated SS-mice (Fig 2G). PubMed:29694434

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MeSH
Liver
MeSH
Anemia, Sickle Cell
Text Location
Results

bp(MESH:"Oxidative Stress") positiveCorrelation a(CHEBI:malonaldehyde) View Subject | View Object

Malondialdehyde (MDA) represents evidence of systemic oxidative stress and inflammation [31], and is commonly used to estimate the level of lipid peroxidation. PubMed:30324533

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MeSH
Hematoma
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Results

bp(MESH:"Oxidative Stress") increases path(MESH:Osteoarthritis) View Subject | View Object

As a part of the inflammatory response after injury, oxidative stress due to formation of reactive oxygen species (ROS) is involved both in direct damage of cartilage components and as integral factors in cell signaling leading to cartilage degradation (Henrotin et al., 2003). PubMed:30505280

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Knee
MeSH
Osteoarthritis, Knee
Text Location
Introduction

bp(MESH:"Oxidative Stress") positiveCorrelation bp(GO:"protein oxidation") View Subject | View Object

Oxidation of proteins result in stable carbonyl groups on amino acid side chains, and protein carbonyl content is one of the most widely used marker of protein oxidation and a general indicator of oxidative stress (Dalle-Donne et al., 2003). PubMed:30505280

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MeSH
Knee
MeSH
Osteoarthritis, Knee
Text Location
Introduction

About

BEL Commons is developed and maintained in an academic capacity by Charles Tapley Hoyt and Daniel Domingo-Fernández at the Fraunhofer SCAI Department of Bioinformatics with support from the IMI project, AETIONOMY. It is built on top of PyBEL, an open source project. Please feel free to contact us here to give us feedback or report any issues. Also, see our Publishing Notes and Data Protection information.

If you find BEL Commons useful in your work, please consider citing: Hoyt, C. T., Domingo-Fernández, D., & Hofmann-Apitius, M. (2018). BEL Commons: an environment for exploration and analysis of networks encoded in Biological Expression Language. Database, 2018(3), 1–11.