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Free Radical Biology and Medicine, ISSN 0891-5849, 07/2012, Volume 53, Issue 2, pp. 260 - 270
Journal Article
Apoptosis, ISSN 1360-8185, 11/2017, Volume 22, Issue 11, pp. 1321 - 1335
Reactive oxygen species (ROS), a group of ions and molecules, include hydroxyl radicals (·OH), alkoxyl radicals, superoxide anion (O2·−), singlet oxygen (1O2)... 
Biochemistry, general | Therapy | Biomedicine | Cell death | ROS | Cancer Research | Oncology | Cell Biology | Virology | Cancer | OXIDATIVE STRESS | INDUCED APOPTOSIS | BIOCHEMISTRY & MOLECULAR BIOLOGY | AUTOPHAGIC CELL-DEATH | P-GLYCOPROTEIN EXPRESSION | ENDOPLASMIC-RETICULUM STRESS | CELL BIOLOGY | MITOCHONDRIAL ROS | NASOPHARYNGEAL CARCINOMA | MEDIATED SONODYNAMIC THERAPY | ROS-DEPENDENT ACTIVATION | T-CELLS | Neoplasms - metabolism | Reactive Oxygen Species - metabolism | Photosensitizing Agents - therapeutic use | Apoptosis - drug effects | Humans | Gene Expression Regulation, Neoplastic | Antineoplastic Agents - therapeutic use | Photochemotherapy | Autophagy - drug effects | Proto-Oncogene Proteins c-akt - genetics | Reactive Oxygen Species - agonists | Mechanistic Target of Rapamycin Complex 1 - genetics | Mitochondria - radiation effects | Neoplasms - radiotherapy | Proto-Oncogene Proteins c-akt - metabolism | Molecular Targeted Therapy - methods | Radiation, Ionizing | Signal Transduction | Necrosis - metabolism | Electron Transport Chain Complex Proteins - genetics | Mitochondria - metabolism | Mitochondria - drug effects | Mechanistic Target of Rapamycin Complex 1 - metabolism | Necrosis - chemically induced | Neoplasms - drug therapy | Electron Transport Chain Complex Proteins - metabolism | Necrosis - genetics | Neoplasms - pathology | Hydrogen peroxide | Hydroxides | Active oxygen | Superoxide | Antineoplastic agents | Cells | Antimitotic agents | Ionizing radiation | Chemotherapy | Immunotherapy | Health aspects | Drugs | Cancer therapies | Immunosuppressive agents | Mammalian cells | Anticancer properties | Mitochondria | Antitumor agents | Hydroxyl radicals | Species | Oxygen | Free radicals | Photodynamic therapy | Mortality | Radiation therapy | Metabolism | Singlet oxygen | Reagents | Electron transport | Apoptosis
Journal Article
Trends in Biotechnology, ISSN 0167-7799, 06/2018, Volume 36, Issue 6, pp. 594 - 602
Journal Article
PLoS ONE, ISSN 1932-6203, 09/2016, Volume 11, Issue 9, pp. e0162497 - e0162497
Microglial priming and enhanced reactivity to secondary insults cause substantial neuronal damage and are hallmarks of brain aging, traumatic brain injury and... 
CELLS | ACTIVATION | PROTEIN | SUPEROXIDE-PRODUCTION | PHOSPHORYLATION | MULTIDISCIPLINARY SCIENCES | PROLIFERATION | ION CHANNELS | K+ CHANNEL | MEDIATED NEUROTOXICITY | NOX2 | Microglia - metabolism | Reactive Oxygen Species - metabolism | Membrane Glycoproteins - metabolism | NADPH Oxidases - metabolism | Peroxynitrous Acid - agonists | Glycoproteins - pharmacology | Reactive Oxygen Species - agonists | Adenosine Triphosphate - pharmacology | Glutathione - agonists | Glutathione - biosynthesis | Membrane Glycoproteins - antagonists & inhibitors | Phenanthrolines - pharmacology | Nitric Oxide Synthase Type II - antagonists & inhibitors | NADPH Oxidases - genetics | Potassium Channels, Inwardly Rectifying - antagonists & inhibitors | Peroxynitrous Acid - antagonists & inhibitors | p38 Mitogen-Activated Protein Kinases - metabolism | Microglia - cytology | NG-Nitroarginine Methyl Ester - pharmacology | Cell Line | Nitric Oxide - biosynthesis | Microglia - drug effects | Signal Transduction | Nitric Oxide - antagonists & inhibitors | NADPH Oxidases - antagonists & inhibitors | Enzyme Inhibitors - pharmacology | Gene Expression Regulation | p38 Mitogen-Activated Protein Kinases - genetics | Glutathione - antagonists & inhibitors | Potassium Channels, Inwardly Rectifying - genetics | Imidazoles - pharmacology | NADPH Oxidase 2 | Nitric Oxide - agonists | Membrane Glycoproteins - genetics | Peroxynitrous Acid - biosynthesis | Reactive Oxygen Species - antagonists & inhibitors | Animals | Nitric Oxide Synthase Type II - genetics | p38 Mitogen-Activated Protein Kinases - antagonists & inhibitors | Acetylcysteine - pharmacology | Mice | Pyridines - pharmacology | Potassium Channels, Inwardly Rectifying - metabolism | Interferon-gamma - pharmacology | Nitric Oxide Synthase Type II - metabolism | Brain | Cell culture | Reactive oxygen species | Traumatic brain injury | Disease | Oxidase | Infections | Experiments | Channels | NAD(P)H oxidase | Neurotoxicity | Head injuries | CYBB protein | Aging | Inhibition | Glutathione | Peroxynitrite | Oxygen | Neurodegenerative diseases | Potassium channels (inwardly-rectifying) | Research & development--R&D | Neutrophils | MAP kinase | Priming | Microglia | NG-Nitroarginine methyl ester | Neurological diseases | Pathology | Brain research | Nitric oxide | γ-Interferon | Brain damage | N-Acetyl-L-cysteine | Interferon | Intracellular | Potassium | Dementia | Index Medicus | Research & development | R&D
Journal Article
Journal Article
Journal of Biological Chemistry, ISSN 0021-9258, 06/2017, Volume 292, Issue 24, pp. 9896 - 9905
Journal Article
PLoS ONE, ISSN 1932-6203, 08/2015, Volume 10, Issue 8, p. e0135083
The chemotherapeutic use of cisplatin is limited by its severe side effects. In this study, by conducting different omics data analyses, we demonstrated that... 
APOPTOSIS | OXIDATIVE STRESS | P53 ACTIVATION | PROTEIN-KINASE | MULTIDISCIPLINARY SCIENCES | TUBULAR EPITHELIAL-CELLS | DOWN-REGULATION | AUDITORY CELLS | DEATH | CANCER | NEPHROTOXICITY | L-Lactate Dehydrogenase - metabolism | Epithelial Cells - metabolism | Reactive Oxygen Species - metabolism | Apoptosis - drug effects | Epithelial Cells - drug effects | Humans | Male | Membrane Potential, Mitochondrial - drug effects | Glycolysis - drug effects | Reactive Oxygen Species - agonists | Tumor Suppressor Protein p53 - genetics | Antineoplastic Agents - toxicity | Dose-Response Relationship, Drug | Cisplatin - toxicity | Tumor Suppressor Protein p53 - agonists | Epithelial Cells - cytology | Kidney Tubules - metabolism | Cell Line | Kidney Tubules - drug effects | Citric Acid Cycle - drug effects | Gene Expression Regulation | Injections, Intraperitoneal | Tumor Suppressor Protein p53 - metabolism | Rats | Rats, Sprague-Dawley | Kidney Tubules - cytology | Animals | L-Lactate Dehydrogenase - genetics | Acetylcysteine - pharmacology | Cell Proliferation - drug effects | Physiological aspects | Reactive oxygen species | Genetic aspects | Research | Cisplatin | Bioengineering | Tricarboxylic acid cycle | Oxidative stress | Correlation | Toxicity | p53 Protein | Genes | Science | Cytotoxicity | Kinases | Ovarian cancer | Mitochondria | Cell growth | Pathways | Metabolites | Rodents | Cell cycle | Inhibition | Adenosine triphosphate | Urine | Abnormalities | Mortality | Data processing | Interdisciplinary aspects | Metabolism | Gene expression | Side effects | Cell death | Glycolysis | Apoptosis
Journal Article
PLoS ONE, ISSN 1932-6203, 07/2013, Volume 8, Issue 7, p. e70210
We have previously reported that Porphyromonas gingivalis infection of gingival epithelial cells (GEC) requires an exogenous danger signal such as ATP to... 
Connexins - antagonists & inhibitors | Gingiva - immunology | RNA, Small Interfering - genetics | Inflammasomes - metabolism | Reactive Oxygen Species - metabolism | NLR Family, Pyrin Domain-Containing 3 Protein | Epithelial Cells - drug effects | Humans | Reactive Oxygen Species - agonists | Receptors, Purinergic P2X7 - genetics | Porphyromonas gingivalis - growth & development | Adenosine Triphosphate - pharmacology | Gingiva - drug effects | Inflammasomes - drug effects | Interleukin-1beta - biosynthesis | Keratinocytes - microbiology | Porphyromonas gingivalis - immunology | Cell Line | Nerve Tissue Proteins - antagonists & inhibitors | Signal Transduction | Gene Expression Regulation | Connexins - genetics | Interleukin-1beta - immunology | Nerve Tissue Proteins - genetics | Keratinocytes - immunology | Connexins - metabolism | Nerve Tissue Proteins - metabolism | Carrier Proteins - genetics | Carrier Proteins - metabolism | Keratinocytes - drug effects | Epithelial Cells - immunology | Epithelial Cells - microbiology | Inflammasomes - immunology | Protein Binding | Receptors, Purinergic P2X7 - metabolism | Primary Cell Culture | Receptors, Purinergic P2X4 - metabolism | Gingiva - microbiology | Receptors, Purinergic P2X4 - genetics | RNA, Small Interfering - metabolism | Pathogens | Health sciences | Reactive oxygen species | Oxygen | Cytokines | Secretion | Purine receptors | Epithelial cells | Interleukin | Caspase | Stimulation | Infections | Activation | Hazards | Biology | IL-1β | Caspase-1 | Proteins | Receptors | Microorganisms | ATP | Apoptosis
Journal Article
Journal Article
PLoS ONE, ISSN 1932-6203, 04/2015, Volume 10, Issue 4, p. e0122398
Vascular tone is controlled by the L-arginine/nitric oxide (NO) pathway, and NO bioavailability is strongly affected by hyperglycaemia-induced oxidative... 
OXIDATIVE STRESS | HYPERGLYCEMIA | MULTIDISCIPLINARY SCIENCES | L-ARGININE TRANSPORT | GESTATIONAL DIABETES-MELLITUS | SLC29A1 PROMOTER ACTIVITY | DYSFUNCTION | TRANSCRIPTION FACTOR | EXPRESSION | CARDIOVASCULAR RISK | ADENOSINE TRANSPORT | Reactive Oxygen Species - metabolism | Human Umbilical Vein Endothelial Cells - metabolism | Humans | Cationic Amino Acid Transporter 1 - metabolism | Spin Labels | Biopterin - analogs & derivatives | Proto-Oncogene Proteins c-akt - genetics | Reactive Oxygen Species - agonists | Biopterin - metabolism | Cyclic N-Oxides - pharmacology | Umbilical Veins - drug effects | Human Umbilical Vein Endothelial Cells - cytology | Mitogen-Activated Protein Kinase 1 - genetics | Acetophenones - pharmacology | Nitric Oxide Synthase Type III - metabolism | Proto-Oncogene Proteins c-akt - metabolism | Vasoconstrictor Agents - pharmacology | Insulin - pharmacology | Human Umbilical Vein Endothelial Cells - drug effects | Signal Transduction | Calcitonin Gene-Related Peptide - pharmacology | Nitric Oxide - antagonists & inhibitors | Tissue Culture Techniques | Gene Expression Regulation | Glucose - pharmacology | Transcription Factors - genetics | Glucose - antagonists & inhibitors | Nitric Oxide Synthase Type III - genetics | Nitric Oxide - agonists | Transcription Factors - metabolism | Reactive Oxygen Species - antagonists & inhibitors | 15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic Acid - pharmacology | Primary Cell Culture | Nitric Oxide - metabolism | Arginine - metabolism | Cationic Amino Acid Transporter 1 - genetics | Mitogen-Activated Protein Kinase 1 - metabolism | Umbilical Veins - metabolism | Oxidases | Nitric oxide | Superoxide | Glucose | Insulin | Phosphotransferases | Dextrose | Endothelium | AKT protein | NAD(P)H oxidase | Vasodilation | Proteins | Hyperglycemia | Synthesis | Physiology | NADPH-diaphorase | Gynecology | Liquid chromatography | Bioavailability | Gene expression | Glucose transport | Potassium chloride | Nitric-oxide synthase | Calcitonin gene-related peptide | Pharmacy | Nicotinamide adenine dinucleotide | Nicotinamide | Transport | Transporter | Oxidative stress | Reactive oxygen species | Phosphorylation | Laboratories | Oxidase | Tempol | Amino acids | Kinases | Contraction | Western blotting | Nerve conduction | Arginine | Calcitonin | Adenosine | Oxygen | Incubation | High-performance liquid chromatography | Obstetrics | Endothelial cells | Medicine | Insulin resistance | Diabetes | Veins & arteries
Journal Article