Search results for "OXIDATION"

showing 10 items of 1913 documents

A role for the peroxisomal 3-ketoacyl-CoA thiolase B enzyme in the control of PPARα-mediated upregulation of SREBP-2 target genes in the liver.: ThB …

2011

International audience; Peroxisomal 3-ketoacyl-CoA thiolase B (Thb) catalyzes the final step in the peroxisomal β-oxidation of straight-chain acyl-CoAs and is under the transcription control of the nuclear hormone receptor PPARα. PPARα binds to and is activated by the synthetic compound Wy14,643 (Wy). Here, we show that the magnitude of Wy-mediated induction of peroxisomal β-oxidation of radiolabeled (1-(14)C) palmitate was significantly reduced in mice deficient for Thb. In contrast, mitochondrial β-oxidation was unaltered in Thb(-/-) mice. Given that Wy-treatment induced Acox1 and MFP-1/-2 activity at a similar level in both genotypes, we concluded that the thiolase step alone was respons…

MaleMESH: HepatomegalyPalmitatesMESH : PyrimidinesMESH : Gene DeletionBiochemistryelement-binding proteinsMESH : Acetyl-CoA C-AcyltransferaseMiceMESH: Up-RegulationMESH: AnimalsMESH : Up-RegulationMESH: Lipid Metabolism0303 health sciencesMESH : Gene Expression RegulationThiolase030302 biochemistry & molecular biologyGeneral MedicineMESH : HepatomegalyUp-Regulationzellweger-syndromePeroxisome ProliferatorsMESH: Peroxisome ProliferatorsHepatomegalySterol Regulatory Element Binding Protein 2peroxisomal 3-ketoacyl-CoA thiolase BMESH: Mitochondria3-oxoacyl-coa thiolaseLathosterolfatty-acid oxidationrat-liverMESH: Sterol Regulatory Element Binding Protein 203 medical and health sciencesMESH : Sterol Regulatory Element Binding Protein 2HumansPPAR alphaMESH : Peroxisome Proliferators[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular BiologyPPARaVLAGMESH : Oxidation-ReductionFatty Acid Oxidation.MESH: HumansCholesterolMESH : HumanscholesterolLipid MetabolismMESH: PeroxisomesSterol regulatory element-binding proteinchemistryMESH: PyrimidinesCholesterol; Micro-array analysis; Peroxisomal 3-ketoacyl-CoA thiolase B; PPARα and SREBP-2; Wy14643Fatty Acid OxidationGene DeletionMESH: LiverMESH: Oxidation-ReductionMESH: Signal TransductionMESH: Mice KnockoutVoeding Metabolisme en Genomicachemistry.chemical_compoundMESH: CholesterolMESH : Lipid MetabolismWy14MESH : PalmitatesMESH: PPAR alphaMESH : CholesterolMice Knockoutneuronal migration643PeroxisomeAcetyl-CoA C-AcyltransferaseMESH: Gene Expression RegulationMetabolism and GenomicsMitochondriaLiverBiochemistryMicro-array analysisMetabolisme en GenomicaACOX1Nutrition Metabolism and GenomicsMESH : MitochondriaOxidation-ReductionSignal Transductionacyl-coa oxidasecholesterol-synthesisMESH : MaleMESH : PPAR alphaPeroxisome ProliferationPPARα and SREBP-2Biologybeta-oxidationVoedingproliferator-activated receptorsMESH : MicePeroxisomesAnimals[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyMESH: Mice030304 developmental biologySCP2NutritionMESH : Signal TransductionMESH : LiverMESH: PalmitatesMESH: MalePyrimidinesMESH: Acetyl-CoA C-AcyltransferaseGene Expression RegulationMESH: Gene DeletionMESH : Mice KnockoutMESH : AnimalsMESH : Peroxisomes
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Free [NADH]/[NAD+] regulates sirtuin expression

2011

Sirtuins are deacetylases involved in metabolic regulation and longevity. Our aim was to test the hypothesis that they are subjected to redox regulation by the [NADH]/[NAD(+)] ratio. We used NIH3T3 fibroblasts in culture, Drosophila fed with or without ethanol and exercising rats. In all three models an increase in [NADH]/[NAD(+)] came up with an increased expression of sirtuin mRNA and protein. PGC-1α (a substrate of sirtuins) protein level was significantly increased in fibroblasts incubated with lactate and pyruvate but this effect was lost in fibroblasts obtained from sirtuin-deficient mice. We conclude that the expression of sirtuins is subject to tight redox regulation by the [NADH]/[…

MaleMetaboliteBiophysicsBiochemistryMicechemistry.chemical_compoundPhysical Conditioning AnimalPyruvic AcidAnimalsSirtuinsLactic AcidRNA MessengerRats WistarEthanol metabolismMolecular BiologyCells CulturedGlyceraldehyde 3-phosphate dehydrogenaseRegulation of gene expressionMessenger RNAEthanolbiologyFibroblastsNADPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaRatsCell biologyDrosophila melanogasterGlycerol-3-phosphate dehydrogenaseGene Expression RegulationchemistryBiochemistrySirtuinNIH 3T3 CellsTrans-Activatorsbiology.proteinNAD+ kinaseOxidation-ReductionTranscription FactorsArchives of Biochemistry and Biophysics
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Metabolic pathways of 4-bromo-2,5-dimethoxyphenethylamine (2C-B): analysis of phase I metabolism with hepatocytes of six species including human

2004

Abstract 4-Bromo-2,5-dimethoxyphenethylamine (2C-B) is a psychoactive designer drug of abuse that is sold under the street names “Venus”, “Bromo”, “Erox”, “XTC” or “Nexus”. Concern has been raised because only little is known about its toxicity and metabolism in humans. In the present study we incubated 2C-B with human, monkey, dog, rabbit, rat and mouse hepatocytes to identify the metabolites formed and to determine possible toxic effects as evidenced by an ATP assay. Our data allow construction of the main metabolic pathways of 2C-B. Oxidative deamination results in the 2-(4-bromo-2,5-dimethoxyphenyl)-ethanol (BDMPE) and 4-bromo-2,5-dimethoxyphenylacetic acid (BDMPAA) metabolites. Additio…

MaleMetaboliteDeaminationMice Inbred StrainsBiologyToxicologyGas Chromatography-Mass SpectrometryRats Sprague-DawleyMicechemistry.chemical_compoundAdenosine TriphosphateDogsSpecies SpecificitymedicineAnimalsHumansCells CulturedDemethylationDose-Response Relationship DrugMolecular Structure25-Dimethoxy-4-MethylamphetamineIllicit DrugsOxidative deaminationMetabolismMiddle AgedRatsMacaca fascicularisMetabolic pathwaymedicine.anatomical_structurechemistryBiochemistryDeaminationHepatocyteHepatocytesRabbitsOxidation-ReductionDrug metabolismToxicology
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Production of T suppressor factor specific for the hapten picryl chloride requires both T suppressor cells and an antigen-specific, genetically restr…

1987

Summary We investigated the requirement for activation of T suppressor cells specific for the hapten picryl chloride and the release of hapten-specific T suppressor factor. Using an in vivo experimental system, we report that activation of T suppressor cells and the consequent release of T suppressor factor required two signals: one was provided by primed T suppressor cells, i.e. spleen cells from mice injected with the tolerogen picrylsulphonic acid, and the other was provided by the specific antigen in the context of H-2 gene products. Mechanisms by which the interaction between these two signals led to activation of T suppressor cells and the production of T suppressor factor, as well as…

MaleMice Inbred StrainsPicryl ChlorideBiologyT-Lymphocytes Regulatorylaw.inventionPicryl chlorideEpitopesMicechemistry.chemical_compoundInterleukin 21AntigenlawSuppressor Factors ImmunologicAnimalsCytotoxic T cellDisulfidesCells CulturedGeneral Environmental ScienceH-2 AntigensLymphokineGeneral MedicineT lymphocyteCell biologychemistryImmunologyGeneral Earth and Planetary SciencesSuppressorFemaleHaptensOxidation-ReductionHaptenSpleenAnnales de l'Institut Pasteur / Immunologie
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AZT induces oxidative damage to cardiac mitochondria: Protective effect of vitamins C and E

2004

Abstract AZT (zidovudine) is a potent inhibitor of HIV replication and a major antiretroviral drug used for AIDS treatment. A major limitation in the use of AZT is the occurrence of severe side effects. The aim of this work was to test whether AZT causes oxidative damage to heart mitochondria and whether this can be prevented by supranutritional doses of antioxidant vitamins. An experimental animal model was used in which mice were treated with AZT for 35 days (10 mg/kg/day) in drinking water. Animals treated with antioxidant vitamins were fed the same diet as controls but supplemented with vitamins C (ascorbic acid, 10 g/ kg diet) and E (α-dl-tocopherol, 0.6 g/kg diet) for 65 days before s…

MaleMitochondrial Diseasesmedicine.medical_treatmentAscorbic AcidOxidative phosphorylationMitochondrionPharmacologyBiologymedicine.disease_causeDNA MitochondrialMitochondria HeartGeneral Biochemistry Genetics and Molecular BiologyLipid peroxidationMiceZidovudinechemistry.chemical_compoundmedicineAnimalsVitamin Eheterocyclic compoundsGeneral Pharmacology Toxicology and PharmaceuticsVitamin CVitamin EDeoxyguanosineGeneral MedicineAscorbic acidGlutathioneBiochemistrychemistry8-Hydroxy-2'-DeoxyguanosineLipid PeroxidationZidovudineOxidative stressmedicine.drugLife Sciences
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Part of the Series: From Dietary Antioxidants to Regulators in Cellular Signalling and Gene ExpressionRole of reactive oxygen species and (phyto)oest…

2006

There is increasing evidence that reactive oxygen species (ROS) are not only toxic but play an important role in cellular signalling and in the regulation of gene expression. We, here, discuss two examples of improved adaptive response to an altered cellular redox state. First, differences in longevity between males and females may be explained by a higher expression of antioxidant enzymes in females resulting in a lower yield of mitochondrial ROS. Oestrogens are made responsible for these phenomena. Oestradiol induces glutathione peroxidase-1 and MnSOD by processes requiring the cell surface oestrogen receptor (ER) and the activation of pathways usually involved in oxidative stress respons…

MaleMitochondrial ROSAgingAntioxidantmedicine.medical_treatmentGene ExpressionPhytoestrogensmedicine.disease_causeBiochemistryAntioxidantsSuperoxide dismutasechemistry.chemical_compoundGlutathione Peroxidase GPX1medicineAnimalsHumansRegulation of gene expressionchemistry.chemical_classificationGlutathione PeroxidaseReactive oxygen speciesEstradiolbiologySuperoxide DismutaseGeneral MedicineGlutathioneCatalaseRatsOxidative StressReceptors EstrogenBiochemistrychemistryCatalaseDietary Supplementsbiology.proteinFemaleReactive Oxygen SpeciesOxidation-ReductionOxidative stressSignal TransductionFree Radical Research
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Analysis of the membrane potential of rat- and mouse-liver mitochondria by flow cytometry and possible applications.

1990

Washed and purified rat- or mouse-liver mitochondria exhibiting high membrane integrity and metabolic activity were studied by flow cytometry. The electrophoretic accumulation/redistribution of cationic lipophilic probes, rhodamine 123, safranine O and a cyanine derivative, 3,3'-dihexyloxadicarbocyanine iodide, during the energization process was studied and was consistent with the generation of a negative internal membrane potential. An exception to this was nonylacridine orange which spontaneously bound to the mitochondrial membrane by hydrophobic interactions via its hydrocarbon chain. Energized purified mitochondria stained with potentiometric dyes exhibited both higher fluorescence and…

MaleNigericinPopulationVoltage-sensitive dyeMitochondria LiverMitochondrionBiologyBiochemistryRhodamine 123Membrane Potentialschemistry.chemical_compoundValinomycinMiceOxygen ConsumptionAmmoniaAnimalsInner mitochondrial membraneeducationFluorescent DyesMembrane potentialeducation.field_of_studyRats Inbred StrainsIntracellular MembranesFlow CytometryRatschemistryBiochemistryOxidation-ReductionEuropean journal of biochemistry
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Oxidative metabolism in a rat hepatoma (N13) and isolated rat hepatocytes: A flow cytometric comparative study

1996

Recently, we have developed a new and fast kinetic method for assessing mitochondrial membrane potential by flow cytometry, based on the quantitation of the initial rate of rhodamine 123 (Rh123) uptake by living cells. This test has proved suitable to detect metabolic and toxic effects on mitochondria. To characterize energy metabolism in a rat hepatoma cell line (N13), we applied this method to assess several metabolic pathways that eventually generate mitochondrial membrane potential. Using this approach, we found that N13 hepatoma cells retain an oxidative capacity comparable with that observed in isolated hepatocytes under the same conditions. These results show that this cell line may …

MaleOrnithineLiver cytologySuccinic AcidOleic AcidsMitochondrionBiologyRhodamine 123Flow cytometrychemistry.chemical_compoundLiver Neoplasms ExperimentalAmmoniaCarnitinemedicineAnimalsRhodamine 123Rats WistarHepatologymedicine.diagnostic_testRhodaminesSuccinatesFlow CytometryIn vitroRatsMetabolic pathwayGlucosemedicine.anatomical_structureLiverBiochemistrychemistryCell cultureHepatocyteGlycolysisOxidation-ReductionOleic AcidHepatology
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Genetically engineered V79 chinese hamster cell expression of purified cytochromeP-450iib1 monooxygenase activity

1989

Chinese hamster V79 fibroblasts, frequently used as target cells in short-term tests for mutagenicity, do not possess measurable monooxygenase activity; in particular, enzymatic oxidation of testosterone (T) cannot be demonstrated. If these V79 cells, however, had been transfected with the cDNA-encoding rat liver cytochrome P-450IIB1 under control of the SV40 early promoter, they stably expressed monooxygenase activity. These so-called SD1 cells then oxidatively metabolized T at a rate of 27 pmol/mg protein/min, converting it to 16 alpha- and 16 beta-hydroxy-T as well as 4-androsten-3,17-dione as sole metabolites in a ratio of 1.1:1.0:1.6. The regio- and stereoselective conversion of T by S…

MaleOxygenaseCytochromeCellTransfectionToxicologyIsozymeChinese hamsterCricetulusCytochrome P-450 Enzyme SystemCricetinaemedicineAnimalsTestosteroneCells CulturedChromatography High Pressure Liquidchemistry.chemical_classificationbiologyRats Inbred StrainsTransfectionKetosteroidsbiology.organism_classificationMolecular biologyRatsIsoenzymesmedicine.anatomical_structureEnzymeBiochemistrychemistryPhenobarbitalMicrosomes LiverOxygenasesbiology.proteinCricetulusGenetic EngineeringOxidation-ReductionJournal of Biochemical Toxicology
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Different brain oxidative and neuroinflammation status in rats during prolonged abstinence depending on their ethanol relapse-like drinking behavior:…

2022

Rationale: Accumulating evidence suggests that chronic alcohol consumption is associated with excessive oxidative damage and neuroinflammatory processes and these events have been associated to early alcohol withdrawal. In the present research we wonder if brain oxidative stress and neuroinflammation remains altered during prolonged withdrawal situations and whether these alterations can be correlated with relapse behavior in alcohol consumption. The effects of alcohol reintroduction were also evaluated Methods: We have used a model based on the alcohol deprivation effect (ADE) within a cohort of wild-type male Wistar rats. Two subpopulations were identified according to the alcohol relapse…

MalePharmacologyAlcohol Efectes fisiològicsAlcohol DrinkingEthanolEstrès oxidatiuPrefrontal CortexToxicologyRatsSubstance Withdrawal SyndromeAlcoholismOxidative StressPsychiatry and Mental healthAlcohol relapseAlcohol deprivation effectNeuroinflammationRecurrenceOxidative stressNeuroinflammatory DiseasesAnimalsPharmacology (medical)Rats WistarOxidation-ReductionCraving
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