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Free Radical Biology and Medicine, ISSN 0891-5849, 07/2017, Volume 108, p. S34
Non-ketotic hyperglycinemia (NKH) is an inborn error of metabolism caused by deficiency in the glycine (GLY) cleavage system and characterized by a high... 
Antioxidants | Phosphates | Enzymes | Evaluation | Physiological aspects | Superoxide | Glycine
Journal Article
Free Radical Biology and Medicine, ISSN 0891-5849, 07/2017, Volume 108, pp. S34 - S34
Journal Article
SCIENTIFIC REPORTS, ISSN 2045-2322, 09/2019, Volume 9, Issue 1, pp. 12651 - 13
Ethylmalonic encephalopathy protein 1 (ETHE1) and molybdenum cofactor (MoCo) deficiencies are hereditary disorders that affect the catabolism of... 
OXIDATIVE STRESS | ENERGY | MOLYBDENUM COFACTOR | RADIATION MITIGATOR JP4-039 | MULTIDISCIPLINARY SCIENCES | HYDROGEN-PEROXIDE | SULFITE OXIDASE DEFICIENCY | DYSFUNCTION | MUTATIONS | ETHYLMALONIC ENCEPHALOPATHY | DISTURBANCE
Journal Article
Journal Article
Molecular Neurobiology, ISSN 0893-7648, 7/2018, Volume 55, Issue 7, pp. 5868 - 5878
Journal Article
Molecular Neurobiology, ISSN 0893-7648, 11/2016, Volume 53, Issue 9, pp. 6459 - 6475
We investigated the effects of an acute intrastriatal QUIN administration on cellular redox and bioenergetics homeostasis, as well as on important signaling... 
Signaling pathways | Neurology | Neurosciences | Energy metabolism | Biomedicine | Glutaric acidemia | Redox homeostasis | Neurobiology | Inflammatory response | Quinolinic acid | Cell Biology | PLASMA-MEMBRANES | 3-HYDROXYGLUTARIC ACID | NMDA RECEPTORS | NITRIC-OXIDE SYNTHASE | FACTOR-KAPPA-B | GLUTAMATE UPTAKE | NEUROSCIENCES | CEREBRAL-CORTEX | PRIMARY NEURONAL CULTURES | ANTIOXIDANT RESPONSE ELEMENT | CREATINE-KINASE | Brain Diseases, Metabolic - pathology | Glutaryl-CoA Dehydrogenase - metabolism | Glutathione - metabolism | Antioxidants - metabolism | Fluoresceins - metabolism | Nitrites - metabolism | NF-kappa B - metabolism | Extracellular Signal-Regulated MAP Kinases - metabolism | Electron Transport Complex IV - metabolism | Amino Acid Metabolism, Inborn Errors - metabolism | Sulfhydryl Compounds - metabolism | Neostriatum - drug effects | Lipid Peroxidation - drug effects | Neostriatum - metabolism | Quinolinic Acid - administration & dosage | Quinolinic Acid - toxicity | Amino Acid Metabolism, Inborn Errors - pathology | Brain Diseases, Metabolic - enzymology | Proto-Oncogene Proteins c-akt - metabolism | Superoxide Dismutase - metabolism | Malondialdehyde - metabolism | Glutathione Peroxidase - metabolism | Neostriatum - pathology | Oxidation-Reduction | Brain Diseases, Metabolic - metabolism | Mice, Knockout | Nitrates - metabolism | Animals | Lactates - metabolism | Diet | Signal Transduction - drug effects | Models, Biological | NF-E2-Related Factor 2 - metabolism | Oxidative Stress - drug effects | Amino Acid Metabolism, Inborn Errors - enzymology | Energy Metabolism - drug effects | Glutaryl-CoA Dehydrogenase - deficiency | Antioxidants | Lysine | Creatine kinase | Glutathione transferase | Physiological aspects | Superoxide | Inflammation | Creatine | Homeostasis | Signal transduction | Oxidative stress | Bioenergetics | Index Medicus
Journal Article
Molecular Neurobiology, ISSN 0893-7648, 1/2019, Volume 56, Issue 1, pp. 29 - 38
Journal Article
Scientific Reports, ISSN 2045-2322, 12/2018, Volume 8, Issue 1, pp. 1165 - 14
Mitochondrial complex I (CI) deficiency is the most frequent cause of oxidative phosphorylation (OXPHOS) disorders in humans. In order to benchmark the effects... 
BETA-OXIDATION | ASSEMBLY FACTOR | NITROXIDE | DEFECTS | METABOLISM | FATTY-ACID OXIDATION | MULTIDISCIPLINARY SCIENCES | HEPG2 CELLS | UBIQUINONE OXIDOREDUCTASE DEFICIENCY | HUMAN NADH | MUTATIONS | Free Radical Scavengers - pharmacology | Mitochondrial Diseases - pathology | Mitochondria - enzymology | Fibroblasts - enzymology | Electron Transport - drug effects | Reactive Oxygen Species - metabolism | Electron Transport - genetics | Electron Transport Complex I - deficiency | Humans | Endoplasmic Reticulum - metabolism | Adenosine Triphosphate - agonists | NADH Dehydrogenase - genetics | Acyl-CoA Dehydrogenases - genetics | Adenosine Triphosphate - biosynthesis | Membrane Potential, Mitochondrial - drug effects | Oxidative Phosphorylation - drug effects | Endoplasmic Reticulum - pathology | Electron Transport Complex I - genetics | Endoplasmic Reticulum - drug effects | Acyl-CoA Dehydrogenases - deficiency | NADH Dehydrogenase - deficiency | Mitochondrial Diseases - genetics | Gene Expression | Mitochondria - drug effects | Mitochondria - pathology | Fibroblasts - pathology | Mitochondrial Diseases - enzymology | Reactive Oxygen Species - antagonists & inhibitors | Fibroblasts - drug effects | Nitrogen Oxides - pharmacology | Primary Cell Culture | NADH-ubiquinone oxidoreductase | Phosphorylation | Reactive oxygen species | Superoxide | Cell interactions | Electron transport chain | Mitochondria | Oxidative phosphorylation | Bioenergetics | Cell lines | Fibroblasts | Membrane potential | Mutation | Electron transport | Endoplasmic reticulum
Journal Article
Molecular Neurobiology, ISSN 0893-7648, 12/2017, Volume 54, Issue 10, pp. 7796 - 7807
Journal Article
Molecular Neurobiology, ISSN 0893-7648, 1/2019, Volume 56, Issue 1, pp. 648 - 657
Journal Article