Its basic function is to protect humans from harmful effects of UV radiation
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Ozone therapy: A clinical review - 0 views
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With viruses, the O3 damages the viral capsid and upsets the reproductive cycle by disrupting the virus-to-cell contact with peroxidation.
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Inactivation of bacteria, viruses, fungi, yeast and protozoa: Ozone therapy disrupts the integrity of the bacterial cell envelope through oxidation of the phospholipids and lipoproteins
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cascade of reactions like peroxidation of lipids leading to changes in membrane permeability,[41] lipid ozonation products (LOP) act as signal transducer molecules
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Dietary antioxidants or free radical scavengers like vitamin E, C, etc., can prevent aforementioned effects of O3
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Lactate metabolism in human lung tumors - 0 views
www.ncbi.nlm.nih.gov/...PMC5684706
lactate MCT mono-carboxylate transporters Cori Cycle lactate metabolism cancer GLUT
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Metabolomic alterations in human cancer cells by vitamin C-induced oxidative stress | S... - 0 views
www.nature.com/...srep13896
GSH vitamin C glutathione glycolysis Pentose phosphate pathway metabolomics PPP TCA cycle H2O2
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NETosis and Neutrophil Extracellular Traps in COVID-19: Immunothrombosis and Beyond - PMC - 0 views
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Pneumonia is a typical symptom of COVID-19 infection, while acute respiratory distress syndrome (ARDS) and multiple organ failure are common in severe COVID-19 patients
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NETs are important for preventing pathogen invasion, their excessive formation can result in a slew of negative consequences, such as autoimmune inflammation and tissue damage
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SARS-CoV-2 infection has also been linked to increased neutrophil-to-lymphocyte ratios, which is associated with disease severity and clinical prognosis
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NETosis is a special form of programmed cell death in neutrophils, which is characterized by the extrusion of DNA, histones, and antimicrobial proteins in a web-like structure known as neutrophil extracellular traps (NETs)
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increased generation of reactive oxygen species (ROS) is a crucial intracellular process that causes NETosis
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In COVID-19, major NET protein cargos of NETs (i.e., NE, MPO, and histones) are significantly elevated.
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SARS-CoV-2 can also infect host cells through noncanonical receptors such as C-type lectin receptors
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Immunopathological manifestations, including cytokine storms and impaired adaptive immunity, are the primary drivers behind COVID-19, with neutrophil infiltration being suggested as a significant cause
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SARS-CoV-2 and its components (e.g., spike proteins and viral RNA) attach to platelets and increase their activation and aggregation in COVID-19, resulting in vascular injury and thrombosis, both of which are linked to NET formation
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NETosis, leading to aberrant immunity such as cytokine storms, autoimmune disorders, and immunosuppression.
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early bacterial coinfections were more prevalent in COVID-19 patients than those infected with other viruses
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NETosis and NETs may also have a role in the development of post COVID-19 syndromes, including lung fibrosis, neurological disorders, tumor growth, and worsening of concomitant disease
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NETs and other by-products of NETosis have been shown to act as direct inflammation amplifiers. Hyperinflammation
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SARS-CoV-2 drives NETosis and NET formation to allow for the release of free DNA and by-products (e.g., elastases and histones). This may trigger surrounding macrophages and endothelial cells to secrete excessive proinflammatory cytokines and chemokines, which, in turn, enhance NET formation and form a positive feedback of cytokine storms in COVID-19
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NET release enables self-antigen exposure and autoantibody production, thereby increasing the autoinflammatory response
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patients with COVID-19 who have higher anti-NET antibodies are more likely to be detected with positive autoantibodies [e.g., antinuclear antibodies (ANA) and anti-neutrophil cytoplasmic antibodies (ANCA)]
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have weakened adaptive immunity as well as a high level of inflammation
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tumor-associated NETosis and NETs promote an immunosuppressive environment in which anti-tumor immunity is compromised
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can enhance this process by interacting with neutrophils through toll-like receptor 4 (TLR4), platelet factor 4 (PF4), and extracellular vesicle-dependent processes
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Following initial onset of COVID-19, an estimated 50% or more of COVID-19 survivors may develop multi-organ problems (e.g., pulmonary dysfunction and neurologic impairment) or have worsening concomitant chronic illness
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NETs in the bronchoalveolar lavage fluid of severe COVID-19 patients cause EMT in lung epithelial cells
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decreased E-cadherin (an epithelial marker) expression
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Patients with tumors have been shown to be more vulnerable to SARS-CoV-2 infection and subsequent development of severe COVID-19
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patients who have recovered from COVID-19 may have an increased risk of developing cancer or of cancer progression and metastasis
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vitamin C has been tested in phase 2 clinical trials aimed at reducing COVID-19-associated mortality by reducing excessive activation of the inflammatory response
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vitamin C is an antioxidant that significantly attenuates PMA-induced NETosis in healthy neutrophils by scavenging ROS
Combining lipoic acid to methylene blue reduces the Warburg effect in CHO cells: From T... - 0 views
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Get All The Answers for Queries Regarding Ovulation - Crysta IVF - 0 views
Curcumin promotes cell cycle arrest and apoptosis of acute myeloid leukemia cells by in... - 0 views
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High-Dose Vitamin C for Cancer Therapy - PMC - 0 views
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diabetes [8], atherosclerosis [9], the common cold [10], cataracts [11], glaucoma [12], macular degeneration [13], stroke [14], heart disease [15], COVID-19 [16], and cancer.
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Iron is found in the human body in the form of haemoglobin in red blood cells and growing erythroid cells.
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iron is taken up by the majority of cells in the form of a transferrin (Tf)-Fe(III) complex that binds to the cell surface receptor transferrin receptor 1 (TfR1)
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the endosomal six transmembrane epithelial antigen of the prostate 3 (STEAP3) reduces Fe(III) (ferric ion) to Fe(II) (ferrous ion), which is subsequently transferred across the endosomal membrane by divalent metal transporter 1 (DMT1)
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DHA is quickly converted to Vit-C within the cell, by interacting with reduced glutathione (GSH) [45,46,47]. NADPH then recycles the oxidized glutathione (glutathione disulfide (GSSG)) and converts it back into GSH
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Fe(II) catalyzes the formation of OH• and OH− during the interaction between H2O2 and O2•− (Haber–Weiss reaction)
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Ascorbate can efficiently reduce free iron, thus recycling the cellular Fe(II)/Fe(III) to produce more OH• from H2O2 than can be generated during the Fenton reaction, which ultimately leads to lipid, protein, and DNA oxidation
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Asc•− and H2O2 were generated in vivo upon i.v Vit-C administration of around 0.5 g/kg of body weight and that the generation was Vit-C-dose reliant
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increase in the expression of various iron-intake pathways or the downregulation of iron exporter proteins and storage pathways
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Advanced breast tumor patients had substantially greater Fe(II) levels in their blood than the control groups without the disease
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Vit-C is supplied, it oxidizes to DHA, and then is readily transported by GLUT-1 in mutant cells of KRAS or BRAF competing with glucose [46]. DHA is quickly converted into ascorbate inside the cell by NADPH and GSH [46,107]. This decrease reduces the concentration of cytosolic antioxidants and raises the intracellular ROS amounts
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ROS activates poly (ADP-ribose) polymerase (PARP), which depletes NAD+ (a critical co-factor of GAPDH); thus, further reducing the GAPDH associated with a multifaceted metabolic rewiring
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high-dose Vit-C recruited metabolites and increased the enzymatic activity in the pentose phosphate pathway (PPP), blocked the tri-carboxylic acid (TCA) cycle, and increased oxygen uptake, disrupting the intracellular metabolic balance and resulting in irreversible cell death, due to an energy crisis
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Due to its great volatility at neutral pH [76], bolus therapy with mega-dose DHA has only transitory effects on tumor cells, both in vitro and in vivo.