ubiquinone has been researched along with Brain-Neoplasms* in 10 studies
1 review(s) available for ubiquinone and Brain-Neoplasms
1 trial(s) available for ubiquinone and Brain-Neoplasms
9 other study(ies) available for ubiquinone and Brain-Neoplasms
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CoQ
Most monotherapies available against glioblastoma multiforme (GBM) target individual hallmarks of this aggressive brain tumor with minimal success. In this article, we propose a therapeutic strategy using coenzyme Q. Xenografts of U251 cells in nu/nu mice were used to assay tumor growth, hypoxia, angiogenesis, and inflammation. An orthotopic model was used to explore microglial infiltration, tumor growth, and invasion into the brain parenchyma. Cell proliferation, migration, invasion, proteome remodeling, and secretome were assayed in vitro. Conditioned media were used to assay angiogenesis, monocyte chemoattraction, and differentiation into macrophages in vitro.. CoQ Topics: Animals; Antioxidants; Brain Neoplasms; Cell Line, Tumor; Glioblastoma; Humans; Hypoxia; Inflammation; Mice; Proteome; Ubiquinone | 2023 |
Modulation of Antioxidant Potential with Coenzyme Q10 Suppressed Invasion of Temozolomide-Resistant Rat Glioma
The main reasons for the inefficiency of standard glioblastoma (GBM) therapy are the occurrence of chemoresistance and the invasion of GBM cells into surrounding brain tissues. New therapeutic approaches obstructing these processes may provide substantial survival improvements. The purpose of this study was to assess the potential of lipophilic antioxidant coenzyme Q10 (CoQ10) as a scavenger of reactive oxygen species (ROS) to increase sensitivity to temozolomide (TMZ) and suppress glioma cell invasion. To that end, we used a previously established TMZ-resistant RC6 rat glioma cell line, characterized by increased production of ROS, altered antioxidative capacity, and high invasion potential. CoQ10 in combination with TMZ exerted a synergistic antiproliferative effect. These results were confirmed in a 3D model of microfluidic devices showing that the CoQ10 and TMZ combination is more cytotoxic to RC6 cells than TMZ monotherapy. In addition, cotreatment with TMZ increased expression of mitochondrial antioxidant enzymes in RC6 cells. The anti-invasive potential of the combined treatment was shown by gelatin degradation, Matrigel invasion, and 3D spheroid invasion assays as well as in animal models. Inhibition of MMP9 gene expression as well as decreased N-cadherin and vimentin protein expression implied that CoQ10 can suppress invasiveness and the epithelial to mesenchymal transition in RC6 cells. Therefore, our data provide evidences in favor of CoQ10 supplementation to standard GBM treatment due to its potential to inhibit GBM invasion through modulation of the antioxidant capacity. Topics: Animals; Antioxidants; Brain Neoplasms; Drug Resistance, Neoplasm; Glioblastoma; Humans; Male; Mice; Rats, Wistar; Temozolomide; Ubiquinone | 2019 |
Regulation of the oxidative balance with coenzyme Q10 sensitizes human glioblastoma cells to radiation and temozolomide.
To investigate how the modulation of the oxidative balance affects cytotoxic therapies in glioblastoma, in vitro.. Human glioblastoma U251 and T98 cells and normal astrocytes C8D1A were loaded with coenzyme Q10 (CoQ). Mitochondrial superoxide ion (O. CoQ did not affect oxygen consumption but reduced the level of O. CoQ acts as sensitizer for cytotoxic therapies, disarming GBM cells, but not normal astrocytes, against further pro-oxidant injuries, being potentially useful in clinical practice for this fatal pathology. Topics: Antioxidants; Apoptosis; Brain Neoplasms; Dacarbazine; DNA Damage; Glioblastoma; Humans; Hydrogen Peroxide; Mitochondria; Oxidative Stress; Oxygen Consumption; Radiation Tolerance; Reactive Oxygen Species; Temozolomide; Tumor Cells, Cultured; Ubiquinone | 2018 |
Hypothalamic digoxin mediated model for oncogenesis.
This study assessed the changes in the isoprenoid pathway and its metabolites digoxin, dolichol and ubiquinone in neoplasms (CNS astrocytomas - glioblastoma multiforme and high grade non - Hodgkin's lymphoma). The following parameters were assessed-isoprenoid pathway metabolites, tyrosine and tryptophan catabolites, glycoconjugate metabolism, RBC membrane composition and free radical metabolism. There was an elevation in plasma HMG CoA reductase activity, serum digoxin and dolichol and a reduction in RBC membrane Na+-K+ ATPase activity, serum ubiquinone and magnesium levels. Serum tryptophan, serotonin, nicotine and quinolinic acid were elevated while tyrosine, dopamine, noradrenaline and morphine were decreased. The total serum glycosaminoglycans and glycosaminoglycan fractions (except dermatan sulphate in the case of CNS astrocytomas), the activity of GAG degrading enzymes and glycohydrolases, carbohydrate residues of glycoproteins and serum glycolipids were elevated. HDL cholesterol showed a significant decrease and free fatty acids & triglycerides were increased. The RBC membrane glycosaminoglycans, hexose and fucose residues of glycoproteins and phospholipids were reduced. The activity of all free radical scavenging enzymes, concentration of glutathione, iron binding capacity and ceruloplasmin decreased significantly while the concentration of malondialdehyde (MDA), hydroperoxides, conjugated dienes and NO increased. The concentration of alpha tocopherol was unaltered. Membrane Na+-K+ ATPase inhibition due to elevated digoxin, altered membrane structure and digoxin related tyrosine / tryptophan transport defect leading to increased levels of depolarising tryptophan catabolites and decreased levels of hyperpolarising tyrosine catabolites can lead to alteration in intracellular calcium/magnesium ratios and oncogene activation. Intracellular magnesium deficiency can produce defective microtubule related spindle fibre dysfunction and chromosomal non-dysjunction contributing to neoplastic cellular polyploidy and aneuploidy. Digoxin induced tryptophan/tyrosine transport defect can alter neurotransmitter patterns with increased serotonin, quinolinic acid, nicotine & glutamatergic transmission and reduced dopamine, morphine and noradrenaline levels leading to oncogenesis. Glycoconjugate metabolism is altered by elevated dolichol levels and magnesium depletion consequent to Na+-K+ ATPase inhibition. There is a qualitative alteration in proteoglycans and glyco Topics: Adult; Astrocytoma; Brain Neoplasms; Cholesterol; Digoxin; Dolichols; Erythrocyte Membrane; Female; Glycosaminoglycans; Humans; Hydroxymethylglutaryl CoA Reductases; Hypothalamus; Lymphoma, Non-Hodgkin; Male; Middle Aged; Signal Transduction; Sodium-Potassium-Exchanging ATPase; Ubiquinone | 2001 |
Tryptophan and tyrosine catabolic pattern in neuropsychiatric disorders.
Catabolism of tryptophan and tyrosine in relation to the isoprenoid pathway was studied in neurological and psychiatric disorders. The concentration of trytophan, quinolinic acid, kynurenic acid, serotonin and 5-hydroxyindoleacetic acid was found to be higher in the plasma of patients with all these disorders; while that of tyrosine, dopamine, epinephrine and norepinephrine was lower. There was increase in free fatty acids and decrease in albumin (factors modulating tryptophan transport) in the plasma of these patients. Concentration of digoxin, a modulator of amino acid transport, and the activity of HMG CoA reductase, which synthesizes digoxin, were higher in these patients; while RBC membrane Na+-K+ ATPase activity showed a decrease. Concentration of plasma ubiquinone (part of which is synthesised from tyrosine) and magnesium was also lower in these patients. No morphine could be detected in the plasma of these patients except in MS. On the other hand, strychnine and nicotine were detectable. These results indicate hypercatabolism of tryptophan and hypocatabolism of tyrosine in these disorders, which could be a consequence of the modulating effect of hypothalamic digoxin on amino acid transport. Topics: Adult; Biogenic Monoamines; Brain Diseases; Brain Neoplasms; Digoxin; Epilepsy, Generalized; Erythrocytes; Fatty Acids, Nonesterified; Female; Glioma; Glycine Agents; Humans; Hydroxymethylglutaryl CoA Reductases; Kynurenic Acid; Magnesium; Male; Microvascular Angina; Middle Aged; Morphine; Narcotics; Nicotine; Nicotinic Agonists; Parkinson Disease; Quinolinic Acid; Schizophrenia; Serum Albumin; Sodium-Potassium-Exchanging ATPase; Strychnine; Tryptophan; Tyrosine; Ubiquinone | 2000 |
Oxidant stress and glioblastoma multiforme risk: serum antioxidants, gamma-glutamyl transpeptidase, and ferritin.
Case-control studies of serum antioxidants are difficult to interpret, because antioxidants may be altered by the disease under study. However, because glioblastoma multiforme (GBM) is a relatively rare disease, a cohort study would require a large sample observed for many years. In the present case-control pilot study (34 cases and 35 controls), we evaluated the association between serum levels of ascorbic acid (AA) and alpha- and gamma-tocopherol (alpha-T and gamma-T) measured before diagnostic surgery. To control for influence of GBM on serum AA, alpha-T, and gamma-T, we adjusted for oxidant stress indexes (gamma-glutamyl transpeptidase and uric acid) and an acute-phase response index (serum ferritin). When adjusted, AA is inversely related to GBM (p for trend = 0.007). In addition, AA interacts with alpha-T to further reduce GBM risk (test for interaction, p = 0.04). gamma-T is not associated with GBM (p = 0.71). However, gamma-glutamyl transpeptidase (p = 0.004), coenzyme Q (p = 0.01), and ferritin (p = 0.009) are positively and uric acid (p = 0.000) is negatively related to GBM. We conclude that 1) AA and alpha-T are jointly related to GBM after adjustment for GBM-produced oxidant stress and 2) there is a strong association between the presence of GBM and oxidant stress. Topics: Acute-Phase Reaction; Aged; alpha-Tocopherol; Antioxidants; Ascorbic Acid; Brain Neoplasms; Case-Control Studies; Female; Ferritins; gamma-Glutamyltransferase; gamma-Tocopherol; Glioblastoma; Humans; Male; Middle Aged; Oxidative Stress; Pilot Projects; Risk Factors; Ubiquinone; Uric Acid | 2000 |
Lipid metabolism as a target for brain cancer therapy: synergistic activity of lovastatin and sodium phenylacetate against human glioma cells.
Malignant gliomas, the most common form of primary brain tumors, are highly dependent on the mevalonate (MVA) pathway for the synthesis of lipid moieties critical to cell replication. Human glioblastoma cells were found to be uniquely vulnerable to growth arrest by lovastatin, a competitive inhibitor of the enzyme regulating MVA synthesis, 3-hydroxy-3-methylglutaryl coenzyme A reductase. The sodium salt of phenylacetic acid (NaPA), an inhibitor of MVA-pyrophosphate decarboxylase, the enzyme that controls MVA use, acted synergistically with lovastatin to suppress malignant growth. When used at pharmacologically attainable concentrations, the two compounds induced profound cytostasis and loss of malignant properties such as invasiveness and expression of the transforming growth factor-beta 2 gene, coding for a potent immunosuppressive cytokine. Supplementation with exogenous ubiquinone, an end product of the MVA pathway, failed to rescue the cells, suggesting that decreased synthesis of intermediary products are responsible for the antitumor effects observed. In addition to blocking the MVA pathway, lovastatin alone and in combination with NaPA increased the expression of the peroxisome proliferator-activated receptor, a transcription factor implicated in the control of lipid metabolism, cell growth, and differentiation. Our results indicate that targeting lipid metabolism with lovastatin, used alone or in combination with the aromatic fatty acid NaPA, may offer a novel approach to the treatment of malignant gliomas. Topics: Antimetabolites, Antineoplastic; Antineoplastic Combined Chemotherapy Protocols; Brain Neoplasms; Cell Division; Drug Synergism; Glioma; Humans; Lipid Metabolism; Lovastatin; Mevalonic Acid; Neoplasm Invasiveness; Phenylacetates; Tumor Cells, Cultured; Ubiquinone | 1996 |
Ubiquinone and nucleic acid concentrations in the heart muscle of cancer patients and normal controls.
Topics: Adult; Aged; Brain Neoplasms; Bronchial Neoplasms; Death, Sudden; DNA; Esophageal Neoplasms; Female; Heart Ventricles; Humans; Male; Middle Aged; Myocardium; Neoplasms; RNA; Stomach Neoplasms; Ubiquinone | 1971 |
Ubiquinone concentrations in some tumour-bearing tissues. Ubiquinone concentrations in tumours and some normal tissues in man.
Topics: Adolescent; Adult; Aged; Brain Neoplasms; Bronchial Neoplasms; Esophageal Neoplasms; Female; Humans; Leukemia, Myeloid; Liver; Lung; Male; Melanoma; Middle Aged; Muscles; Pancreas; Pancreatic Neoplasms; Rectal Neoplasms; Ubiquinone; Uterine Neoplasms | 1966 |