Reactive Oxygen Species
Oxygen
Oxidative Stress
Hydrogen Peroxide
Antioxidants
NADPH Oxidase
Free Radical Scavengers
Mitochondria
Oxygen Consumption
Superoxide Dismutase
Oxidation-Reduction
Catalase
Acetylcysteine
Superoxides
Oxidants
Apoptosis
Membrane Potential, Mitochondrial
Glutathione
Cells, Cultured
Signal Transduction
Lipid Peroxidation
Onium Compounds
Reactive Nitrogen Species
Singlet Oxygen
Xanthine Oxidase
Cell Survival
Cell Death
Free Radicals
Nitric Oxide
Enzyme Activation
DNA Damage
Glutathione Peroxidase
Enzyme Inhibitors
Dose-Response Relationship, Drug
Rats, Sprague-Dawley
Ascorbic Acid
Blotting, Western
1,2-Dihydroxybenzene-3,5-Disulfonic Acid Disodium Salt
Luminescent Measurements
Respiratory Burst
Cytochromes c
Xanthine
Mitochondrial Proteins
Vitamin K 3
Oxygen Inhalation Therapy
Caspase 3
Models, Biological
Electron Transport Complex I
Mice, Knockout
Peroxiredoxins
Metalloporphyrins
Caspases
Neutrophils
Endothelium, Vascular
Protein Carbonylation
Cell Respiration
Electron Transport
NF-E2-Related Factor 2
Spin Labels
Paraquat
Rats, Wistar
NF-kappa B
Phosphorylation
RNA, Messenger
Up-Regulation
DNA Fragmentation
NADH, NADPH Oxidoreductases
p38 Mitogen-Activated Protein Kinases
Disease Models, Animal
Cytoprotection
Thioredoxins
tert-Butylhydroperoxide
rac1 GTP-Binding Protein
Gene Expression Regulation
Calcium
Uncoupling Agents
RNA, Small Interfering
Heme Oxygenase-1
Endothelial Cells
Mitochondrial Membranes
Glutathione Disulfide
Plant Extracts
Thiobarbituric Acid Reactive Substances
Deferoxamine
Fluoresceins
Reverse Transcriptase Polymerase Chain Reaction
Buthionine Sulfoximine
Gene Expression Regulation, Enzymologic
Glucose
Myocytes, Cardiac
Mutation
Antimycin A
Peroxynitrous Acid
Oxidoreductases
Flow Cytometry
Autophagy
Amitrole
Reperfusion Injury
Glutathione Reductase
Mitogen-Activated Protein Kinases
Hypoxia-Inducible Factor 1, alpha Subunit
Iron
Electron Transport Complex II
Electron Spin Resonance Spectroscopy
Electron Transport Chain Complex Proteins
DNA, Mitochondrial
Down-Regulation
Peroxides
Luminol
Necrosis
Macrophages
JNK Mitogen-Activated Protein Kinases
Photosensitizing Agents
Stress, Physiological
Adenosine Triphosphate
Fibroblasts
Tumor Necrosis Factor-alpha
bcl-2-Associated X Protein
Aging
Plant Leaves
Electron Transport Complex III
Arabidopsis
Gene Expression
Peroxidase
Myocardium
RNA Interference
NADP
Cell Aging
Epithelial Cells
Extracellular Signal-Regulated MAP Kinases
Mitochondrial Membrane Transport Proteins
Proto-Oncogene Proteins c-bcl-2
Gene Expression Regulation, Plant
Naphthoquinones
Lung
Nitric Oxide Synthase
HL-60 Cells
Ascorbate Peroxidases
Oxygen Isotopes
Angiotensin II
Inflammation
Nitric Oxide Synthase Type III
Ubiquinone
Vitamin E
Microscopy, Confocal
Lipid Peroxides
Hyperbaric Oxygenation
Thiourea
Neutrophil Activation
Proto-Oncogene Proteins c-akt
Organoselenium Compounds
Oxidative Phosphorylation
Ultraviolet Rays
Cytosol
Membrane Potentials
L-Lactate Dehydrogenase
Neurons
Microscopy, Fluorescence
MAP Kinase Signaling System
Homeostasis
Comet Assay
Hypochlorous Acid
Poly(ADP-ribose) Polymerases
Ethidium
Energy Metabolism
Peroxiredoxin VI
Molecular Sequence Data
Spin Trapping
Heme Oxygenase (Decyclizing)
Oxides
Photochemotherapy
Reactive oxygen intermediate-dependent NF-kappaB activation by interleukin-1beta requires 5-lipoxygenase or NADPH oxidase activity. (1/16336)
We previously reported that the role of reactive oxygen intermediates (ROIs) in NF-kappaB activation by proinflammatory cytokines was cell specific. However, the sources for ROIs in various cell types are yet to be determined and might include 5-lipoxygenase (5-LOX) and NADPH oxidase. 5-LOX and 5-LOX activating protein (FLAP) are coexpressed in lymphoid cells but not in monocytic or epithelial cells. Stimulation of lymphoid cells with interleukin-1beta (IL-1beta) led to ROI production and NF-kappaB activation, which could both be blocked by antioxidants or FLAP inhibitors, confirming that 5-LOX was the source of ROIs and was required for NF-kappaB activation in these cells. IL-1beta stimulation of epithelial cells did not generate any ROIs and NF-kappaB induction was not influenced by 5-LOX inhibitors. However, reintroduction of a functional 5-LOX system in these cells allowed ROI production and 5-LOX-dependent NF-kappaB activation. In monocytic cells, IL-1beta treatment led to a production of ROIs which is independent of the 5-LOX enzyme but requires the NADPH oxidase activity. This pathway involves the Rac1 and Cdc42 GTPases, two enzymes which are not required for NF-kappaB activation by IL-1beta in epithelial cells. In conclusion, three different cell-specific pathways lead to NF-kappaB activation by IL-1beta: a pathway dependent on ROI production by 5-LOX in lymphoid cells, an ROI- and 5-LOX-independent pathway in epithelial cells, and a pathway requiring ROI production by NADPH oxidase in monocytic cells. (+info)Hyperoxia induces the neuronal differentiated phenotype of PC12 cells via a sustained activity of mitogen-activated protein kinase induced by Bcl-2. (2/16336)
We previously reported that rat pheochromocytoma PC12 cells express the neuronal differentiated phenotype under hyperoxia through the production of reactive oxygen species (ROS). In the present study, we found that in this phenotype, Bcl-2, an apoptosis inhibitor, affects mitogen-activated protein (MAP)-kinase activity, which is known as a key enzyme of the signal-transduction cascade for differentiation. When PC12 cells were cultured under hyperoxia, a rapid increase in MAP-kinase activity, including that of both p42 and p44, was observed. Although the activity level then decreased quickly, activity higher than the control level was observed for 48 h. PD98059, an inhibitor of MAP kinase, suppressed the hyperoxia-induced neurite extensions, suggesting the involvement of MAP-kinase activity in the mechanism of differentiation induced by ROS. An elevation of Bcl-2 expression was observed after culturing PC12 cells for 24 h under hyperoxia. This Bcl-2 elevation was not affected by treatment with PD98059, suggesting that it did not directly induce neurite extension under hyperoxia. However, the blockade of the Bcl-2 elevation by an antisense oligonucleotide inhibited the sustained MAP-kinase activity and neurite extensions under hyperoxia. Further, in PC12 cells highly expressing Bcl-2, the sustained MAP-kinase activity and neurite extensions under hyperoxia were enhanced. These results suggested that MAP kinase is activated through the production of ROS, and the subsequent elevation of Bcl-2 expression sustains the MAP-kinase activity, resulting in the induction of the neuronal-differentiation phenotype of PC12 cells under hyperoxia. (+info)The Pseudomonas aeruginosa secretory product pyocyanin inactivates alpha1 protease inhibitor: implications for the pathogenesis of cystic fibrosis lung disease. (3/16336)
Alpha1 Protease inhibitor (alpha1PI) modulates serine protease activity in the lung. Reactive oxygen species inactivate alpha1PI, and this process has been implicated in the pathogenesis of a variety of forms of lung injury. An imbalance of protease-antiprotease activity is also detected in the airways of patients with cystic fibrosis-associated lung disease who are infected with Pseudomonas aeruginosa. P. aeruginosa secretes pyocyanin, which, through its ability to redox cycle, induces cells to generate reactive oxygen species. We tested the hypothesis that redox cycling of pyocyanin could lead to inactivation of alpha1PI. When alpha1PI was exposed to NADH and pyocyanin, a combination that results in superoxide production, alpha1PI lost its ability to form an inhibitory complex with both porcine pancreatic elastase (PPE) and trypsin. Similarly, addition of pyocyanin to cultures of human airway epithelial cells to which alpha1PI was also added resulted in a loss of the ability of alpha1PI to form a complex with PPE or trypsin. Neither superoxide dismutase, catalase, nor dimethylthiourea nor depletion of the media of O2 to prevent formation of reactive oxygen species blocked pyocyanin-mediated inactivation of alpha1PI. These data raise the possibility that a direct interaction between reduced pyocyanin and alpha1PI is involved in the process. Consistent with this possibility, pretreatment of alpha1PI with the reducing agent beta-mercaptoethanol also inhibited binding of trypsin to alpha1PI. These data suggest that pyocyanin could contribute to lung injury in the P. aeruginosa-infected airway of cystic fibrosis patients by decreasing the ability of alpha1PI to control the local activity of serine proteases. (+info)Inflammatory cell-mediated tumour progression and minisatellite mutation correlate with the decrease of antioxidative enzymes in murine fibrosarcoma cells. (4/16336)
We isolated six clones of weakly tumorigenic fibrosarcoma (QR) from the tumorigenic clone BMT-11 cl-9. The QR clones were unable to grow in normal C57BL/6 mice when injected s.c. (1x10(5) cells). However, they formed aggressive tumours upon co-implantation with a 'foreign body', i.e. a gelatin sponge, and the rate of tumour take ranged from 8% to 58% among QR clones. The enhanced tumorigenicity was due to host cell-mediated reaction to the gelatin sponge (inflammation). Immunoblot analysis and enzyme activity assay revealed a significant inverse correlation between the frequencies of tumour formation by QR clones and the levels of manganese superoxide dismutase (Mn-SOD, P<0.005) and glutathione peroxidase (GPchi, P<0.01) in the respective tumour clones. Electron spin resonance (ESR) revealed that superoxide-scavenging ability of cell lysates of the QR clone with high level of Mn-SOD was significantly higher than that with low level of the antioxidative enzyme in the presence of potassium cyanide, an inhibitor for copper-zinc superoxide dismutase (CuZn-SOD) (P<0.001). Minisatellite mutation (MSM) induced by the inflammatory cells in tumour cells were investigated by DNA fingerprint analysis after QR clones had been co-cultured with gelatin-sponge-reactive cells. The MSM rate was significantly higher in the subclones with low levels of Mn-SOD and GPchi (P<0.05) than in the subclones with high levels of both enzymes. The MSM of the subclones with low levels of both enzymes was inhibited in the presence of mannitol, a hydroxyl radical scavenger. The content of 8-hydroxydeoxyguanosine (8-OHdG) by which the cellular DNA damage caused by active oxygen species can be assessed was significantly low in the tumours arising from the QR clone with high levels of Mn-SOD and GPchi even if the clone had been co-implanted with gelatin sponge, compared with the arising tumour from the QR clone with low levels of those antioxidative enzymes (P<0.001). In contrast, CuZn-SOD and catalase levels in the six QR clones did not have any correlation with tumour progression parameters. These results suggest that tumour progression is accelerated by inflammation-induced active oxygen species particularly accompanied with declined levels of intracellular antioxidative enzymes in tumour cells. (+info)Reactive oxygen species play an important role in the activation of heat shock factor 1 in ischemic-reperfused heart. (5/16336)
BACKGROUND: The myocardial protective role of heat shock protein (HSP) has been demonstrated. Recently, we reported that ischemia/reperfusion induced a significant activation of heat shock factor (HSF) 1 and an accumulation of mRNA for HSP70 and HSP90. We examined the role of reactive oxygen species (ROSs) in the induction of stress response in the ischemic-reperfused heart. METHODS AND RESULTS: Rat hearts were isolated and perfused with Krebs-Henseleit buffer by the Langendorff method. Whole-cell extracts were prepared for gel mobility shift assay using oligonucleotides containing the heat shock element. Induction of mRNA for HSP70 and HSP90 was examined by Northern blot analysis. Repetitive ischemia/reperfusion, which causes recurrent bursts of free radical generation, resulted in burst activation of HSF1, and this burst activation was significantly reduced with either allopurinol 1 mmol/L (an inhibitor of xanthine oxidase) or catalase 2x10(5) U/L (a scavenger of H2O2). Significant activation of HSF1 was observed on perfusion with buffer containing H2O2 150 micromol/L or xanthine 1 mmol/L plus xanthine oxidase 5 U/L. The accumulation of mRNA for HSP70 or HSP90 after repetitive ischemia/reperfusion was reduced with either allopurinol or catalase. CONCLUSIONS: Our findings demonstrate that ROSs play an important role in the activation of HSF1 and the accumulation of mRNA for HSP70 and HSP90 in the ischemic-reperfused heart. (+info)Methemoglobin formation by hydroxylamine metabolites of sulfamethoxazole and dapsone: implications for differences in adverse drug reactions. (6/16336)
Differences in the incidence of adverse drug reactions to trimethoprim-sulfamethoxazole and dapsone may result from differences in the formation, disposition, toxicity, and/or detoxification of their hydroxylamine metabolites. In this study, we examine whether differences in the biochemical processing of sulfamethoxazole hydroxylamine (SMX-NOH) and dapsone hydroxylamine (DDS-NOH) by erythrocytes [red blood cells (RBCs)] contribute to this differential incidence. The methemoglobin (MetHgb)-forming capacity of both metabolites was compared after a 60-min incubation with washed RBCs from four healthy human volunteers. DDS-NOH was significantly more potent (P =.004) but equally efficacious with SMX-NOH in its ability to form MetHgb. The elimination of potential differences in disposition by lysing RBCs did not change the MetHgb-forming potency of either hydroxylamine. At pharmacologically relevant concentrations, greater reduction to the parent amine occurred with DDS-NOH. Maintenance of MetHgb-forming potency was dependent on recycling with glutathione, but no difference in cycling efficiency was observed between DDS-NOH and SMX-NOH. In contrast, the pharmacodynamics of hydroxylamine-induced MetHgb formation were not changed by pretreatment with the glucose 6-phosphate dehydrogenase inhibitor epiandrosterone or by compounds that alter normal antioxidant enzyme activity. Methylene blue, which stimulates NADPH-dependent MetHgb reductase activity, decreased MetHgb levels but did not alter the differential potency of these hydroxylamines. DDS-NOH was also significantly more potent when incubated with purified human hemoglobin A0. Collectively, these data suggest that the inherently greater reactivity of DDS-NOH with hemoglobin, the greater conversion of DDS-NOH to its parent amine, and potential differences in disposition of hydroxylamine metabolites may contribute to the preferential development of dapsone-induced hemotoxicity and sulfamethoxazole-induced hypersensitivity reactions. (+info)Mechanisms and mediators in coal dust induced toxicity: a review. (7/16336)
Chronic inhalation of coal dust can cause several lung disorders, including simple coal workers pneumoconiosis (CWP), progressive massive fibrosis (PMF), chronic bronchitis, lung function loss, and emphysema. This review focuses on the cellular actions and interactions of key inflammatory cells and target cells in coal dust toxicity and related lung disorders, i.e. macrophages and neutrophils, epithelial cells, and fibroblasts. Factors released from or affecting these cells are outlined in separate sections, i.e. (1) reactive oxygen species (ROS) and related antioxidant protection mechanisms, and (2) cytokines, growth factors and related proteins. Furthermore, (3) components of the extracellular matrix (ECM), including the modifying role of ROS, cytokines, proteases and antiproteases are discussed in relation to tissue damage and remodelling in the respiratory tract. It is recognised that inhaled coal dust particles are important non-cellular and cellular sources of ROS in the lung, and may be significantly involved in the damage of lung target cells as well as important macromolecules including alpha-1-antitrypsin and DNA. In vitro and in vivo studies with coal dusts showed the up-regulation of important leukocyte recruiting factors, e.g. Leukotriene-B4 (LTB4), Platelet Derived Growth Factor (PDGF), Monocyte Chemotactic Protein-1 (MCP-1), and Tumor Necrosis Factor-alpha (TNF alpha), as well as the neutrophil adhesion factor Intercellular Adhesion Molecule-1 (ICAM-1). Coal dust particles are also known to stimulate the (macrophage) production of various factors with potential capacity to modulate lung cells and/or extracellular matrix, including O2-., H2O2, and NO, fibroblast chemoattractants (e.g. Transforming Growth Factor-beta (TGF beta), PDGF, and fibronectin) and a number of factors that have been shown to stimulate and/or inhibit fibroblast growth or collagen production such as (TNF alpha, TGF beta, PDGF, Insulin Like Growth Factor, and Prostaglandin-E2). Further studies are needed to clarify the in vivo kinetics and relative impact of these factors. (+info)1,25-Dihydroxyvitamin D3 enhances the susceptibility of breast cancer cells to doxorubicin-induced oxidative damage. (8/16336)
1,25-Dihydroxyvitamin D3 (1,25(OH)2D3), the hormonal form of vitamin D, has anticancer activity in vivo and in vitro. Doxorubicin exerts its cytotoxic effect on tumor cells mainly by two mechanisms: (a) generation of reactive oxygen species (ROS); and (b) inhibition of topoisomerase II. We studied the combined cytotoxic action of 1,25(OH)2D3 and doxorubicin on MCF-7 breast cancer cells. Pretreatement with 1,25(OH)2D3 resulted in enhanced cytotoxicity of doxorubicin. The average enhancing effect after a 72-h pretreatment with 1,25(OH)2D3 (10 nM) followed by a 24-h treatment with 1 microg/ml doxorubicin was 74+/-9% (mean +/- SE). Under these experimental conditions, 1,25(OH)2D3 on its own did not affect cell number or viability. 1,25(OH)2D3 also enhanced the cytotoxic activity of another ROS generating quinone, menadione, but did not affect cytotoxicity induced by the topoisomerase inhibitor etoposide. The antioxidant N-acetylcysteine slightly reduced the cytotoxic activity of doxorubicin but had a marked protective effect against the combined action of 1,25(OH)2D3 and doxorubicin. These results indicate that ROS are involved in the interaction between 1,25(OH)2D3 and doxorubicin. 1,25(OH)2D3 also increased doxorubicin cytotoxicity in primary cultures of rat cardiomyocytes. Treatment of MCF-7 cells with 1,25(OH)2D3 alone markedly reduced the activity, protein, and mRNA levels of the cytoplasmic antioxidant enzyme Cu/Zn superoxide dismutase, which indicated that the hormone inhibits its biosynthesis. This reduction in the antioxidant capacity of the cells could account for the synergistic interaction between 1,25(OH)2D3 and doxorubicin and may also suggest increased efficacy of 1,25(OH)2D3 or its analogues in combination with other ROS-generating anticancer therapeutic modalities. (+info)There are different types of anoxia, including:
1. Cerebral anoxia: This occurs when the brain does not receive enough oxygen, leading to cognitive impairment, confusion, and loss of consciousness.
2. Pulmonary anoxia: This occurs when the lungs do not receive enough oxygen, leading to shortness of breath, coughing, and chest pain.
3. Cardiac anoxia: This occurs when the heart does not receive enough oxygen, leading to cardiac arrest and potentially death.
4. Global anoxia: This is a complete lack of oxygen to the entire body, leading to widespread tissue damage and death.
Treatment for anoxia depends on the underlying cause and the severity of the condition. In some cases, hospitalization may be necessary to provide oxygen therapy, pain management, and other supportive care. In severe cases, anoxia can lead to long-term disability or death.
Prevention of anoxia is important, and this includes managing underlying medical conditions such as heart disease, diabetes, and respiratory problems. It also involves avoiding activities that can lead to oxygen deprivation, such as scuba diving or high-altitude climbing, without proper training and equipment.
In summary, anoxia is a serious medical condition that occurs when there is a lack of oxygen in the body or specific tissues or organs. It can cause cell death and tissue damage, leading to serious health complications and even death if left untreated. Early diagnosis and treatment are crucial to prevent long-term disability or death.
1) They share similarities with humans: Many animal species share similar biological and physiological characteristics with humans, making them useful for studying human diseases. For example, mice and rats are often used to study diseases such as diabetes, heart disease, and cancer because they have similar metabolic and cardiovascular systems to humans.
2) They can be genetically manipulated: Animal disease models can be genetically engineered to develop specific diseases or to model human genetic disorders. This allows researchers to study the progression of the disease and test potential treatments in a controlled environment.
3) They can be used to test drugs and therapies: Before new drugs or therapies are tested in humans, they are often first tested in animal models of disease. This allows researchers to assess the safety and efficacy of the treatment before moving on to human clinical trials.
4) They can provide insights into disease mechanisms: Studying disease models in animals can provide valuable insights into the underlying mechanisms of a particular disease. This information can then be used to develop new treatments or improve existing ones.
5) Reduces the need for human testing: Using animal disease models reduces the need for human testing, which can be time-consuming, expensive, and ethically challenging. However, it is important to note that animal models are not perfect substitutes for human subjects, and results obtained from animal studies may not always translate to humans.
6) They can be used to study infectious diseases: Animal disease models can be used to study infectious diseases such as HIV, TB, and malaria. These models allow researchers to understand how the disease is transmitted, how it progresses, and how it responds to treatment.
7) They can be used to study complex diseases: Animal disease models can be used to study complex diseases such as cancer, diabetes, and heart disease. These models allow researchers to understand the underlying mechanisms of the disease and test potential treatments.
8) They are cost-effective: Animal disease models are often less expensive than human clinical trials, making them a cost-effective way to conduct research.
9) They can be used to study drug delivery: Animal disease models can be used to study drug delivery and pharmacokinetics, which is important for developing new drugs and drug delivery systems.
10) They can be used to study aging: Animal disease models can be used to study the aging process and age-related diseases such as Alzheimer's and Parkinson's. This allows researchers to understand how aging contributes to disease and develop potential treatments.
Reperfusion injury can cause inflammation, cell death, and impaired function in the affected tissue or organ. The severity of reperfusion injury can vary depending on the duration and severity of the initial ischemic event, as well as the promptness and effectiveness of treatment to restore blood flow.
Reperfusion injury can be a complicating factor in various medical conditions, including:
1. Myocardial infarction (heart attack): Reperfusion injury can occur when blood flow is restored to the heart muscle after a heart attack, leading to inflammation and cell death.
2. Stroke: Reperfusion injury can occur when blood flow is restored to the brain after an ischemic stroke, leading to inflammation and damage to brain tissue.
3. Organ transplantation: Reperfusion injury can occur when a transplanted organ is subjected to ischemia during harvesting or preservation, and then reperfused with blood.
4. Peripheral arterial disease: Reperfusion injury can occur when blood flow is restored to a previously occluded peripheral artery, leading to inflammation and damage to the affected tissue.
Treatment of reperfusion injury often involves medications to reduce inflammation and oxidative stress, as well as supportive care to manage symptoms and prevent further complications. In some cases, experimental therapies such as stem cell transplantation or gene therapy may be used to promote tissue repair and regeneration.
Hyperoxia can cause damage to the body's tissues and organs, particularly the lungs and brain. In severe cases, hyperoxia can lead to respiratory failure, seizures, and even death.
There are several ways to diagnose hyperoxia, including:
1. Blood tests: These can measure the levels of oxygen in the blood.
2. Arterial blood gas (ABG) analysis: This is a test that measures the amounts of oxygen and carbon dioxide in the blood.
3. Pulse oximetry: This is a non-invasive test that measures the amount of oxygen in the blood by shining a light through the skin.
Treatment for hyperoxia depends on the underlying cause, but may include:
1. Oxygen therapy: This involves administering oxygen to the patient through a mask or nasal tubes.
2. Medications: These may be used to treat any underlying conditions that are causing hyperoxia.
3. Mechanical ventilation: In severe cases, this may be necessary to support the patient's breathing.
In summary, hyperoxia is a condition where there is too much oxygen in the body, and it can cause damage to the body's tissues and organs. Diagnosis is typically made through blood tests or other tests, and treatment may involve oxygen therapy, medications, or mechanical ventilation.
Necrosis is a type of cell death that occurs when cells are exposed to excessive stress, injury, or inflammation, leading to damage to the cell membrane and the release of cellular contents into the surrounding tissue. This can lead to the formation of gangrene, which is the death of body tissue due to lack of blood supply.
There are several types of necrosis, including:
1. Coagulative necrosis: This type of necrosis occurs when there is a lack of blood supply to the tissues, leading to the formation of a firm, white plaque on the surface of the affected area.
2. Liquefactive necrosis: This type of necrosis occurs when there is an infection or inflammation that causes the death of cells and the formation of pus.
3. Caseous necrosis: This type of necrosis occurs when there is a chronic infection, such as tuberculosis, and the affected tissue becomes soft and cheese-like.
4. Fat necrosis: This type of necrosis occurs when there is trauma to fatty tissue, leading to the formation of firm, yellowish nodules.
5. Necrotizing fasciitis: This is a severe and life-threatening form of necrosis that affects the skin and underlying tissues, often as a result of bacterial infection.
The diagnosis of necrosis is typically made through a combination of physical examination, imaging studies such as X-rays or CT scans, and laboratory tests such as biopsy. Treatment depends on the underlying cause of the necrosis and may include antibiotics, surgical debridement, or amputation in severe cases.
There are several key features of inflammation:
1. Increased blood flow: Blood vessels in the affected area dilate, allowing more blood to flow into the tissue and bringing with it immune cells, nutrients, and other signaling molecules.
2. Leukocyte migration: White blood cells, such as neutrophils and monocytes, migrate towards the site of inflammation in response to chemical signals.
3. Release of mediators: Inflammatory mediators, such as cytokines and chemokines, are released by immune cells and other cells in the affected tissue. These molecules help to coordinate the immune response and attract more immune cells to the site of inflammation.
4. Activation of immune cells: Immune cells, such as macrophages and T cells, become activated and start to phagocytose (engulf) pathogens or damaged tissue.
5. Increased heat production: Inflammation can cause an increase in metabolic activity in the affected tissue, leading to increased heat production.
6. Redness and swelling: Increased blood flow and leakiness of blood vessels can cause redness and swelling in the affected area.
7. Pain: Inflammation can cause pain through the activation of nociceptors (pain-sensing neurons) and the release of pro-inflammatory mediators.
Inflammation can be acute or chronic. Acute inflammation is a short-term response to injury or infection, which helps to resolve the issue quickly. Chronic inflammation is a long-term response that can cause ongoing damage and diseases such as arthritis, asthma, and cancer.
There are several types of inflammation, including:
1. Acute inflammation: A short-term response to injury or infection.
2. Chronic inflammation: A long-term response that can cause ongoing damage and diseases.
3. Autoimmune inflammation: An inappropriate immune response against the body's own tissues.
4. Allergic inflammation: An immune response to a harmless substance, such as pollen or dust mites.
5. Parasitic inflammation: An immune response to parasites, such as worms or fungi.
6. Bacterial inflammation: An immune response to bacteria.
7. Viral inflammation: An immune response to viruses.
8. Fungal inflammation: An immune response to fungi.
There are several ways to reduce inflammation, including:
1. Medications such as nonsteroidal anti-inflammatory drugs (NSAIDs), corticosteroids, and disease-modifying anti-rheumatic drugs (DMARDs).
2. Lifestyle changes, such as a healthy diet, regular exercise, stress management, and getting enough sleep.
3. Alternative therapies, such as acupuncture, herbal supplements, and mind-body practices.
4. Addressing underlying conditions, such as hormonal imbalances, gut health issues, and chronic infections.
5. Using anti-inflammatory compounds found in certain foods, such as omega-3 fatty acids, turmeric, and ginger.
It's important to note that chronic inflammation can lead to a range of health problems, including:
1. Arthritis
2. Diabetes
3. Heart disease
4. Cancer
5. Alzheimer's disease
6. Parkinson's disease
7. Autoimmune disorders, such as lupus and rheumatoid arthritis.
Therefore, it's important to manage inflammation effectively to prevent these complications and improve overall health and well-being.
MRI can occur in various cardiovascular conditions, such as myocardial infarction (heart attack), cardiac arrest, and cardiac surgery. The severity of MRI can range from mild to severe, depending on the extent and duration of the ischemic event.
The pathophysiology of MRI involves a complex interplay of various cellular and molecular mechanisms. During ischemia, the heart muscle cells undergo changes in energy metabolism, electrolyte balance, and cell membrane function. When blood flow is restored, these changes can lead to an influx of calcium ions into the cells, activation of enzymes, and production of reactive oxygen species (ROS), which can damage the cells and their membranes.
The clinical presentation of MRI can vary depending on the severity of the injury. Some patients may experience chest pain, shortness of breath, and fatigue. Others may have more severe symptoms, such as cardiogenic shock or ventricular arrhythmias. The diagnosis of MRI is based on a combination of clinical findings, electrocardiography (ECG), echocardiography, and cardiac biomarkers.
The treatment of MRI is focused on addressing the underlying cause of the injury and managing its symptoms. For example, in patients with myocardial infarction, thrombolysis or percutaneous coronary intervention may be used to restore blood flow to the affected area. In patients with cardiac arrest, cardiopulmonary resuscitation (CPR) and other life-saving interventions may be necessary.
Prevention of MRI is crucial in reducing its incidence and severity. This involves aggressive risk factor management, such as controlling hypertension, diabetes, and dyslipidemia, as well as smoking cessation and stress reduction. Additionally, patients with a history of MI should adhere to their medication regimen, which may include beta blockers, ACE inhibitors or ARBs, statins, and aspirin.
In conclusion, myocardial injury with ST-segment elevation (MRI) is a life-threatening condition that requires prompt recognition and treatment. While the clinical presentation can vary depending on the severity of the injury, early diagnosis and management are crucial in reducing morbidity and mortality. Prevention through aggressive risk factor management and adherence to medication regimens is also essential in preventing MRI.
Mitochondrial diseases can affect anyone, regardless of age or gender, and they can be caused by mutations in either the mitochondrial DNA (mtDNA) or the nuclear DNA (nDNA). These mutations can be inherited from one's parents or acquired during embryonic development.
Some of the most common symptoms of mitochondrial diseases include:
1. Muscle weakness and wasting
2. Seizures
3. Cognitive impairment
4. Vision loss
5. Hearing loss
6. Heart problems
7. Neurological disorders
8. Gastrointestinal issues
9. Liver and kidney dysfunction
Some examples of mitochondrial diseases include:
1. MELAS syndrome (Mitochondrial Myopathy, Encephalopathy, Lactic Acidosis, and Stroke-like episodes)
2. Kearns-Sayre syndrome (a rare progressive disorder that affects the nervous system and other organs)
3. Chronic progressive external ophthalmoplegia (CPEO), which is characterized by weakness of the extraocular muscles and vision loss
4. Mitochondrial DNA depletion syndrome, which can cause a wide range of symptoms including seizures, developmental delays, and muscle weakness.
5. Mitochondrial myopathy, encephalomyopathy, lactic acidosis, and stroke-like episodes (MELAS)
6. Leigh syndrome, which is a rare genetic disorder that affects the brain and spinal cord.
7. LHON (Leber's Hereditary Optic Neuropathy), which is a rare form of vision loss that can lead to blindness in one or both eyes.
8. Mitochondrial DNA mutation, which can cause a wide range of symptoms including seizures, developmental delays, and muscle weakness.
9. Mitochondrial myopathy, encephalomyopathy, lactic acidosis, and stroke-like episodes (MELAS)
10. Kearns-Sayre syndrome, which is a rare progressive disorder that affects the nervous system and other organs.
It's important to note that this is not an exhaustive list and there are many more mitochondrial diseases and disorders that can affect individuals. Additionally, while these diseases are rare, they can have a significant impact on the quality of life of those affected and their families.
Types of Experimental Diabetes Mellitus include:
1. Streptozotocin-induced diabetes: This type of EDM is caused by administration of streptozotocin, a chemical that damages the insulin-producing beta cells in the pancreas, leading to high blood sugar levels.
2. Alloxan-induced diabetes: This type of EDM is caused by administration of alloxan, a chemical that also damages the insulin-producing beta cells in the pancreas.
3. Pancreatectomy-induced diabetes: In this type of EDM, the pancreas is surgically removed or damaged, leading to loss of insulin production and high blood sugar levels.
Experimental Diabetes Mellitus has several applications in research, including:
1. Testing new drugs and therapies for diabetes treatment: EDM allows researchers to evaluate the effectiveness of new treatments on blood sugar control and other physiological processes.
2. Studying the pathophysiology of diabetes: By inducing EDM in animals, researchers can study the progression of diabetes and its effects on various organs and tissues.
3. Investigating the role of genetics in diabetes: Researchers can use EDM to study the effects of genetic mutations on diabetes development and progression.
4. Evaluating the efficacy of new diagnostic techniques: EDM allows researchers to test new methods for diagnosing diabetes and monitoring blood sugar levels.
5. Investigating the complications of diabetes: By inducing EDM in animals, researchers can study the development of complications such as retinopathy, nephropathy, and cardiovascular disease.
In conclusion, Experimental Diabetes Mellitus is a valuable tool for researchers studying diabetes and its complications. The technique allows for precise control over blood sugar levels and has numerous applications in testing new treatments, studying the pathophysiology of diabetes, investigating the role of genetics, evaluating new diagnostic techniques, and investigating complications.
Neoplasm refers to an abnormal growth of cells that can be benign (non-cancerous) or malignant (cancerous). Neoplasms can occur in any part of the body and can affect various organs and tissues. The term "neoplasm" is often used interchangeably with "tumor," but while all tumors are neoplasms, not all neoplasms are tumors.
Types of Neoplasms
There are many different types of neoplasms, including:
1. Carcinomas: These are malignant tumors that arise in the epithelial cells lining organs and glands. Examples include breast cancer, lung cancer, and colon cancer.
2. Sarcomas: These are malignant tumors that arise in connective tissue, such as bone, cartilage, and fat. Examples include osteosarcoma (bone cancer) and soft tissue sarcoma.
3. Lymphomas: These are cancers of the immune system, specifically affecting the lymph nodes and other lymphoid tissues. Examples include Hodgkin lymphoma and non-Hodgkin lymphoma.
4. Leukemias: These are cancers of the blood and bone marrow that affect the white blood cells. Examples include acute myeloid leukemia (AML) and chronic lymphocytic leukemia (CLL).
5. Melanomas: These are malignant tumors that arise in the pigment-producing cells called melanocytes. Examples include skin melanoma and eye melanoma.
Causes and Risk Factors of Neoplasms
The exact causes of neoplasms are not fully understood, but there are several known risk factors that can increase the likelihood of developing a neoplasm. These include:
1. Genetic predisposition: Some people may be born with genetic mutations that increase their risk of developing certain types of neoplasms.
2. Environmental factors: Exposure to certain environmental toxins, such as radiation and certain chemicals, can increase the risk of developing a neoplasm.
3. Infection: Some neoplasms are caused by viruses or bacteria. For example, human papillomavirus (HPV) is a common cause of cervical cancer.
4. Lifestyle factors: Factors such as smoking, excessive alcohol consumption, and a poor diet can increase the risk of developing certain types of neoplasms.
5. Family history: A person's risk of developing a neoplasm may be higher if they have a family history of the condition.
Signs and Symptoms of Neoplasms
The signs and symptoms of neoplasms can vary depending on the type of cancer and where it is located in the body. Some common signs and symptoms include:
1. Unusual lumps or swelling
2. Pain
3. Fatigue
4. Weight loss
5. Change in bowel or bladder habits
6. Unexplained bleeding
7. Coughing up blood
8. Hoarseness or a persistent cough
9. Changes in appetite or digestion
10. Skin changes, such as a new mole or a change in the size or color of an existing mole.
Diagnosis and Treatment of Neoplasms
The diagnosis of a neoplasm usually involves a combination of physical examination, imaging tests (such as X-rays, CT scans, or MRI scans), and biopsy. A biopsy involves removing a small sample of tissue from the suspected tumor and examining it under a microscope for cancer cells.
The treatment of neoplasms depends on the type, size, location, and stage of the cancer, as well as the patient's overall health. Some common treatments include:
1. Surgery: Removing the tumor and surrounding tissue can be an effective way to treat many types of cancer.
2. Chemotherapy: Using drugs to kill cancer cells can be effective for some types of cancer, especially if the cancer has spread to other parts of the body.
3. Radiation therapy: Using high-energy radiation to kill cancer cells can be effective for some types of cancer, especially if the cancer is located in a specific area of the body.
4. Immunotherapy: Boosting the body's immune system to fight cancer can be an effective treatment for some types of cancer.
5. Targeted therapy: Using drugs or other substances to target specific molecules on cancer cells can be an effective treatment for some types of cancer.
Prevention of Neoplasms
While it is not always possible to prevent neoplasms, there are several steps that can reduce the risk of developing cancer. These include:
1. Avoiding exposure to known carcinogens (such as tobacco smoke and radiation)
2. Maintaining a healthy diet and lifestyle
3. Getting regular exercise
4. Not smoking or using tobacco products
5. Limiting alcohol consumption
6. Getting vaccinated against certain viruses that are associated with cancer (such as human papillomavirus, or HPV)
7. Participating in screening programs for early detection of cancer (such as mammograms for breast cancer and colonoscopies for colon cancer)
8. Avoiding excessive exposure to sunlight and using protective measures such as sunscreen and hats to prevent skin cancer.
It's important to note that not all cancers can be prevented, and some may be caused by factors that are not yet understood or cannot be controlled. However, by taking these steps, individuals can reduce their risk of developing cancer and improve their overall health and well-being.
There are several types of ischemia, including:
1. Myocardial ischemia: Reduced blood flow to the heart muscle, which can lead to chest pain or a heart attack.
2. Cerebral ischemia: Reduced blood flow to the brain, which can lead to stroke or cognitive impairment.
3. Peripheral arterial ischemia: Reduced blood flow to the legs and arms.
4. Renal ischemia: Reduced blood flow to the kidneys.
5. Hepatic ischemia: Reduced blood flow to the liver.
Ischemia can be diagnosed through a variety of tests, including electrocardiograms (ECGs), stress tests, and imaging studies such as CT or MRI scans. Treatment for ischemia depends on the underlying cause and may include medications, lifestyle changes, or surgical interventions.
Reactive oxygen species
Reactive oxygen species production in marine microalgae
Polyol pathway
DNA repair
Oxidative stress
Pardaxin
Sperm Chromatin Structure Assay
Respiratory complex I
Protein carbonylation
Ergothioneine
Catalase
Respiratory burst
MTORC1
T cell
Reverse electron flow
Endothelial activation
Cardiovascular disease in women
KRIT1
Almokalant
S-Nitrosoglutathione
Anthocyanin
Fumonisin B1
Neurotoxin
Abscission
Malondialdehyde
Peroxisome
Tissue engineering of heart valves
Isoprene
Semen quality
Ashok Agarwal
Hyporheic zone
Death-associated protein 6
Halobacterium salinarum
Metabolism
NOX4
Extractive metallurgy
Senescence
Sodium-potassium pump
Pascal J. Goldschmidt
Lutzomyia longipalpis
Mitochondrial DNA
Streptomyces natalensis
Grassing (textiles)
Aflatoxin B1
Listener fatigue
YopE protein domain
Biophoton
Biometal (biology)
Herbal medicine
5-Hydroxyuracil
Porphyrin
Sodium hypochlorite
High-entropy alloy
Ammonia
Histatin
Bioluminescence
Cellulose
P16
Sonogashira coupling
Blakeslea trispora
Mitochondrial reactive oxygen species regulate the induction of CD8+ T cells by plasmacytoid dendritic cells | Nature...
The epigenetic landscape related to reactive oxygen species formation in the cardiovascular system
Antioxidants | Free Full-Text | Cigarette Smoke Extract Activates Hypoxia-Inducible Factors in a Reactive Oxygen Species...
"Reactive Oxygen Species (ROS) mediated degradation of organophosphate " by Timothy J Nicodemus, Concetta C. DiRusso et al.
Is alpha-lipoic acid a scavenger of reactive oxygen species in vivo? Evidence for its initiation of stress signaling pathways...
Aminoguanidine inhibits reactive oxygen species formation, lipid peroxidation, and oxidant-induced apoptosis. | Scholars@Duke
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| Reactive Oxygen Species
Mitochondrial Reactive Oxygen Species Generation Initiates the Hypoxic Pulmonary Vasoconstriction Response - Northwestern...
Reactive oxygen species | Pharmacognosy Journal
Reactive Oxygen Species | DC Chemicals
Hybrid vesicles as intracellular reactive oxygen species and nitric oxide generators - Forskning - Aarhus Universitet
Reactive oxygen species: friends and foes of signal transduction.
Reactive Oxygen Species
Sies H, Jones DP: Reactive oxygen species (ROS) as pleiotropic physiological signalling agents. Nat Rev Mol Cell Biol 21(7):...
Redox Homeostasis and Cellular Antioxidant Systems: Crucial Players in Cancer Growth and Therapy
Pharmaceutics | Special Issue : Recent Progress in Reactive Oxygen Species-Related Therapy for Disease Treatment
Nitric oxide reactive oxygen species their interplay and detoxification in Neisseria meningitidis
- York Research Database
SUMO E3 ligase SIZ1 connects sumoylation and reactive oxygen species homeostasis processes in Arabidopsis. | Plant Physiol;189...
Frontiers | Luteolin Prevents UVB-Induced Skin Photoaging Damage by Modulating SIRT3/ROS/MAPK Signaling: An in vitro and in...
Do reactive oxygen species regulate skeletal muscle glucose uptake during contraction? | VU Research Repository | Victoria...
Involvement of Induced Resistance by Methyl Jasmonate to Bacterial Wilt and Reactive Oxygen Species Metabolism in Pepper...
Effects of Alkaline Stress on the Metabolism of Reactive Oxygen Species and Osmotica Accumulation in Ryegrass Seedling Roots
Interplay between Reactive Oxygen/Reactive Nitrogen Species and Metabolism in Vascular Biology and Disease<...
Reactive Oxygen Species Stimulate Insulin Secretion in Rat Pancreatic Islets: Studies Using Mono-Oleoyl-Glycerol • MatTek Life...
Intracellular Reactive Oxygen Species Mediate the Therapeutic Effect of Induced Pluripotent Stem Cells for Acute Kidney Injury ...
An Overview of Melatonin as an Antioxidant Molecule: A Biochemical Approach | IntechOpen
PDF) Vitamin Para-Aminobenzoic Acid (PABA) Controls Generation of Nitric Oxide (NO) In Vitro and its Biological Functions in...
8-Hydroxy-2'-Deoxyguanosine and Reactive Oxygen Species as Biomarkers of Oxidative Stress in Mental Illnesses: A Meta-Analysis
Intracellular2
- In this study, the effects of preincubation with AG on oxidant-induced apoptosis, oxidant-induced intracellular reactive oxygen species (ROS) production, and lipid peroxidation were determined in rat retinal Müller cells and compared with the effects of NGF, a protein that protects neuronal cells from oxidative stress. (duke.edu)
- The maintenance of highly regulated mechanisms to control intracellular levels of reactive oxygen species (ROS) is essential for normal cellular homeostasis. (unisi.it)
Apoptosis2
- Aminoguanidine inhibits reactive oxygen species formation, lipid peroxidation, and oxidant-induced apoptosis. (duke.edu)
- Diallyl Trisulfide suppresses the growth of Penicillium expansum (MFC99 value: ≤ 90 μg/mL) and promotes apoptosis via production of reactive oxygen species (ROS) and disintegration of cellular ultrastructure. (dcchemicals.com)
Proteins2
- H 2 O 2 is the more stable and diffusible form of ROS, it is selectively reactive towards cysteine residues on proteins, and, in the low nanomolar range, it can control cellular signaling (Figure 1 ). (hindawi.com)
- This lack of reactive oxygen species causes the body to overcompensate by activating more immune cells and producing more immune proteins. (medlineplus.gov)
Oxidative3
- A significant number of studies now show that LA and its reduced form, dihydrolipoic acid (DHLA), directly scavenge reactive oxygen species (ROS) and reactive nitrogen species (RNS) species and protect cells against a host of insults where oxidative stress is part of the underlying etiology. (oregonstate.edu)
- Electron spin resonance and flow cytometry studies showed that superoxide is the primary oxidative species induced by DOX and responsible for the death inducing effect. (cdc.gov)
- Recent source of free radicals8 which can also deplete study carried out by a local research body, scavengers of reactive oxygen species (ROS), indicated an increase in the rate of teenage accentuating oxidative damage9. (who.int)
Nitric oxide1
- Effects of Exogenous Nitric Oxide on Active Oxygen Metabolism, Polyamine Content and Photosynthesis of Ryegrass( Lolium perenne L.) Seedlings Under Salt Stress [J]. Bulletin of Botanical Research, 2009, 29(3): 313-319. (nefu.edu.cn)
Metabolism5
- To explore the relationship between methyl jasmonate(MeJA)-induced resistance to bacterial wilt and enzymes related to reactive oxygen species metabolism in pepper,the susceptible variety'Yuehong 1'and resistant variety'Xinxiang 8'were used as the experimental materials in the study. (ahs.ac.cn)
- The indexes of bacterial wilt,the activities of enzymes related to reactive oxygen species(ROS)metabolism including superoxide dismutase(SOD),catalase(CAT),peroxidase(POD)and ascorbate peroxidase(APX),and the contents of malondialdehyde(MDA)were determined. (ahs.ac.cn)
- These results suggested that MeJA induced resistance to bacterial wilt in pepper seedlings,and the increased activities of enzymes related to reactive oxygen species metabolism and the decreased lipid peroxidation might be involved in this resistance induction. (ahs.ac.cn)
- To explore the tolerant extent of ryegrass seedlings to alkaline stress, ryegrass seedlings were exposed to Hoagland's nutrient solution with NaHCO 3 added (0, 50, 100, 150, 200 mmol·L -1 ), and the effects of NaHCO 3 stress on the growth of roots, metabolism of reactive oxygen species (ROS) and osmotica accumulation in roots were studied by a sandy culture in greenhouse. (nefu.edu.cn)
- Effects of KCl on Active Oxygen Metabolism and Osmotica Accumulation in Avena nude L. Seedlings under NaCl Stress [J]. Bulletin of Botanical Research, 2015, 35(2): 233-239. (nefu.edu.cn)
Superoxide1
- This enzyme participates in a chemical reaction that converts oxygen to a toxic molecule called superoxide. (medlineplus.gov)
Scavenger2
- Is alpha-lipoic acid a scavenger of reactive oxygen species in vivo? (oregonstate.edu)
- 5-Galloylquinic acid, an main scavenger of the reactive oxygen species (ROS) in green tea. (dcchemicals.com)
Regulate1
- Do reactive oxygen species regulate skeletal muscle glucose uptake during contraction? (edu.au)
Homeostasis1
- SUMO E3 ligase SIZ1 connects sumoylation and reactive oxygen species homeostasis processes in Arabidopsis. (bvsalud.org)
Toxic2
- This study found that metabolically active cultures of the microalga C. subellipsoidea breakdown organophosphates (paraoxon, malathion and diazinon) with differing structural conformations in freshwater through a mechanism that requires the formation of reactive oxygen species (ROS) with little to no toxic effects on the algae. (unl.edu)
- These highly reactive, toxic substances are known as reactive oxygen species. (medlineplus.gov)
Molecules2
- Reactive oxygen species (ROS) can act as damaging molecules but also represent central hubs in cellular signalling networks. (nih.gov)
- Reactive oxygen species (ROS) are highly reactive molecules that are principally derived from the oxygen that is consumed in various metabolic reactions occurring mainly in the mitochondria, peroxisomes, and the endoplasmic reticulum. (hindawi.com)
Mechanism1
- Here we show that the induction of cross-presentation by pDCs is regulated by mitochondria through a reactive oxygen species (ROS)-dependent mechanism, involving pH alkalization and antigen protection. (nature.com)
Cells3
- RAW264.7 cells exposed to MMA-SS had elevated generation of reactive oxygen species (ROS), protein-HNE (P-HNE) adduct formation, activation of ERK1/2, and expression of cyclooxygenase-2 (COX-2) compared to GMA-MS and control. (cdc.gov)
- Treatment of the cells with DOX induced reactive oxygen species (ROS) generation and a concomitant increase in apoptotic cell death through the mitochondrial death pathway independent of p53. (cdc.gov)
- The in vitro effects of metronidazole on the production of reactive oxygen species by polymorphonuclear [PMN] cells were studied by means of nitroblue tetrazolium and luminol-dependent chemiluminescence. (who.int)
Metals1
- Signaling by carcinogenic metals and metal-induced reactive oxygen species. (cdc.gov)
Immune1
- As a result, fewer reactive oxygen species are produced when foreign invaders trigger an immune reaction. (medlineplus.gov)
Physiological2
- Sies H, Jones DP: Reactive oxygen species (ROS) as pleiotropic physiological signalling agents. (iuf-duesseldorf.de)
- Reactive oxygen species (ROS) as pleiotropic physiological signalling agents. (iuf-duesseldorf.de)
Generation2
- Ensulizole can damage the DNA through the generation of reactive oxygen species (ROS) upon UV or sunlight irradiation. (dcchemicals.com)
- Generation of reactive oxygen species by silicon nanowires. (cdc.gov)
Invaders1
- As a result, phagocytes are unable to produce reactive oxygen species to kill foreign invaders and neutrophil activity is not regulated. (medlineplus.gov)
Formation1
- Tetrahydroxyquinone hydrate can take part in a redox cycle with semiquinone radicals, leading to the formation of reactive oxygen species (ROS). (dcchemicals.com)
Production5
- Camalexin can induce reactive oxygen species (ROS) production. (dcchemicals.com)
- D-α-Hydroxyglutaric acid increases reactive oxygen species (ROS) production. (dcchemicals.com)
- Buprofezin also dose-dependently increases the production of reactive oxygen species (ROS) in vitro. (dcchemicals.com)
- A common feature of many of these external stresses is the production of reactive oxygen species (ROS). (bvsalud.org)
- At therapeutic doses of metronidazole [4.98-24.86 microg/mL] significant inhibition of the production of reactive oxygen species was noted in both methods. (who.int)
Levels1
- Skin damage was observed using hematoxylin-eosin (HE) and Masson staining, skin and cellular reactive oxygen species (ROS) levels were detected by DHE and DCF fluorescent probes, mitochondrial membrane potential was detected by JC-1 staining, and protein expressions were detected by immunofluorescence and Western Blot. (frontiersin.org)
Host1
- The next largest category (6 articles) included papers describing evolutionary selection pressures on infectious organisms, either in the natural environment or in host species. (cdc.gov)
Known as reactive oxygen2
- These highly reactive, toxic substances are known as reactive oxygen species. (medlineplus.gov)
- Stressors trigger the cell to make what are known as reactive oxygen species. (nih.gov)
Prodrug1
- Reactive Oxygen Species Activatable Heterodimeric Prodrug as Tumor-Selective Nanotheranostics. (nih.gov)
Inhibits2
NADPH1
- The formation of reactive oxygen species (ROS) by the myeloid cell NADPH oxidase NOX2 is critical for the destruction of engulfed microorganisms. (nih.gov)
Superoxide2
- This enzyme participates in a chemical reaction that converts oxygen to a toxic molecule called superoxide. (medlineplus.gov)
- The semiubiquinones, being unstable, are prone to transfer one electron to molecular oxygen to form superoxide, providing a possible mechanism for Cd-induced generation of ROS in mitochondria. (cdc.gov)
Cancer1
- Reactive oxygen species (ROS) have been implicated in the pathogenesis of cancer. (cdc.gov)
Trigger1
- As a result, fewer reactive oxygen species are produced when foreign invaders trigger an immune reaction. (medlineplus.gov)
Immune1
- This lack of reactive oxygen species causes the body to overcompensate by activating more immune cells and producing more immune proteins. (medlineplus.gov)
Effects4
- The precise mechanism of action of sulfasalazine and/or its metabolites has not been completely elucidated, though its antioxidant effects are well established and are probably due to its scavenging effects against reactive oxygen and nitrogen species (ROS and RNS), as well as metal chelating properties, in association to its inhibitory effects over neutrophil oxidative burst. (nih.gov)
- Reactive oxygen species (ROS) have been shown to have tissue-damaging effects that underlie many disease complications, including those associated with diabetes, Parkinson's, Alzheimer's, and atherosclerosis (Brownlee, 2005). (nih.gov)
- What are the molecular mechanisms that moderate the differential effects of different biochemical species of dietary lipids, such as palmitate and linoleic acid, on tumor progression? (nih.gov)
- We investigated the effects of Cd on the individual complexes of the electron transfer chain (ETC) and on the stimulation of reactive oxygen species (ROS) production in mitochondria. (cdc.gov)
Cell1
- Methionine-misacylation, then, may benefit the cell by protecting proteins from reactive oxygen species. (nih.gov)
Activity1
- As a result, phagocytes are unable to produce reactive oxygen species to kill foreign invaders and neutrophil activity is not regulated. (medlineplus.gov)