Search results for "Oxidation."

showing 10 items of 1877 documents

Hepatic metabolism of diallyl disulfide in rat and man

2003

International audience; 1. The metabolism of diallyl disulphide was investigated in vitro with rat and human liver cell subfractions and ex vivo with an isolated perfused rat liver. 2. Diallyl disulphide was oxidized to diallylthiosulphinate by rat liver microsomes with an apparent K-m = 0.86 +/- 0.1 mM and an apparent V-max = 0.47 +/- 0.12 nmol min(-1) mg(-1) protein (mean +/- SE). Both cytochrome P450 (CYP) and flavin-containing monooxygenases were involved, with CYP2B1/2 and CYP2E1 being the most active CYP enzymes. 3. In rat and man, microsomal oxidation of allylmethyl sulphide to allylmethyl sulphoxide and allylmethyl sulphone also occurred, although at a low rate. Diallyl disulphide w…

MaleLIVERHealth Toxicology and MutagenesisToxicologyBiochemistryGARLICchemistry.chemical_compoundDisulfides0303 health sciencesbiologyDADS030302 biochemistry & molecular biologyCytochrome P-450 CYP2E1General MedicineCYP2E1Middle Agedfoie3. Good healthEnzymesAllyl CompoundsPerfusionBiochemistryArea Under CurveMicrosomes LiverFemaleAryl Hydrocarbon HydroxylasesOxidation-Reductionailcomposé soufrexénobiotique[SDV.BID]Life Sciences [q-bio]/BiodiversityIn Vitro Techniques03 medical and health sciencesAnimalsHumansmétabolisme030304 developmental biologyAgedPharmacologySulfur CompoundsEX VIVOCytochrome P450SULFUR COMPOUNDMetabolismGlutathioneMonooxygenaseRatschemistryDADS;EX VIVO;SULFUR COMPOUND;XENOBIOTIC METABOLISM;GARLIC;LIVER;RATCytochrome P-450 CYP2B1Steroid HydroxylasesMicrosomebiology.proteinRATAllyl MercaptanXENOBIOTIC METABOLISMDrug metabolism
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Pathway of alpha-linolenic acid through the mitochondrial outer membrane in the rat liver and influence on the rate of oxidation. Comparison with lin…

1989

The movement of alpha-linolenic acid (C18:3, n-3) through the mitochondrial outer membrane to oxidation sites was studied in rat liver and compared with the movement of linoleic acid (C18:2, n-6) and oleic acid (C18:1, n-9). All differ in the degree of unsaturation, but have the same chain length and the same position of the first double bond when counted from the carboxyl end. The following results were obtained. (1) The overall beta-oxidation in total mitochondria was in the order C18:3, n-3 greater than C18:2, n-6 greater than C18:1, n-9, independent of the amount of albumin in the medium. (2) The rate of formation of acylcarnitine from acyl-CoA was higher with oleoyl-CoA than with linol…

MaleLinolenic AcidsLinoleic acidPotassiumchemistry.chemical_elementMitochondria LiverOleic AcidsMitochondrionIn Vitro TechniquesBiochemistryLinoleic Acidchemistry.chemical_compoundCarnitinemedicineAnimalsCarnitineMolecular BiologyDegree of unsaturationCarnitine O-PalmitoyltransferaseChemistryalpha-Linolenic acidBiological TransportRats Inbred StrainsCell BiologyIntracellular MembranesPeroxisomeRatsOleic acidBiochemistryLinoleic Acidslipids (amino acids peptides and proteins)Acyl Coenzyme AOxidation-Reductionmedicine.drugOleic AcidResearch ArticleThe Biochemical journal
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Quantitative evaluation of ethane and n-pentane as indicators of lipid peroxidation in vivo.

1983

The use of exhalation of ethane and n-pentane in experimental animals as parameters of lipid peroxidation led to an examination of pharmacokinetics of both compounds in rats. When rats were exposed, in a closed desiccator jar chamber, to a wide range of ethane concentrations, linear elimination pharmacokinetics were observed. n-Pentane, when concentrations higher than 100 ppm were applied, displayed saturation kinetics. These were formally explained by action of two competing metabolizing pathways or enzymes. Application of preexisting models could describe exhalation of both ethane and n-pentane by untreated control rats. Stimulation of lipid peroxidation by ferrous ions or by carbon tetra…

MaleLipid PeroxidesChromatography GasHealth Toxicology and MutagenesisIronKineticsInorganic chemistryPentanesToxicologyLipid peroxidationchemistry.chemical_compoundPharmacokineticsPentanesAnimalsCarbon TetrachlorideEthaneChromatographyExhalationRats Inbred StrainsGeneral MedicineMetabolismRatsPentaneKineticschemistryBreath TestsCarbon tetrachlorideArchives of toxicology
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4-Hydroxynonenal, a lipid peroxidation product, induces relaxation of human cerebral arteries.

1994

The relaxant effect of 4-hydroxynonenal (4-HNE), a lipid peroxidation product, on human cerebral arteries was studied. Addition of 4-HNE to artery rings promoted no contraction, and after stimulation with prostaglandin F2α (PFG2α; 10−7-3 × 10−6 M), 100% relaxation was obtained with 3 × 10−5 M 4-HNE. Inhibition of nitric oxide formation with NG-nitro-l-arginine methyl ester hydrochloride (l-NAME; (10−4 M), as well as prostaglandin synthesis with indomethacin (3 × 10−6 M), partially prevented 4-HNE-induced relaxation, but each of these substances separately failed to inhibit complete relaxation. Addition of both inhibitors together reduced 4-HNE-induced relaxation to ≈50%, but relaxation cou…

MaleLipid PeroxidesContraction (grammar)EndotheliumIndomethacinCerebral arteriesStimulationVasodilationArginineDinoprostNitric Oxide4-HydroxynonenalNitric oxideLipid peroxidationchemistry.chemical_compoundCadavermedicineHumansAgedAged 80 and overAldehydesDose-Response Relationship DrugChemistryOsmolar ConcentrationCerebral ArteriesMiddle AgedVasodilationNG-Nitroarginine Methyl Estermedicine.anatomical_structureNeurologyBiochemistryBiophysicsEndothelium VascularNeurology (clinical)Cardiology and Cardiovascular Medicine
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Effect of acidosis and anoxia on iron delocalization from brain homogenates.

1992

Abstract Cortical homogenates were prepared from rat brain in Krebs-Ringer phosphate media adjusted to pH 7, 6 or 5 and incubated for 1 hr under aerotic or anaerobic conditions in the presence of dipyridyl, an iron chelator. Low molecular weight species (LMWS) iron was measured spectrophotometrically after passing of the homogenates through a 10,000- M , ultrafiltration membrane. Following aerobic incubation, LMWS iron reached 1.24 μg/g tissue at pH 7, and increased 1.7-fold at pH 6 and 3.1-fold at pH 5. Anoxia enhanced significantly the amount of ultrafiltrable iron at the three pH values, the LMWS iron level being increased by 190% at pH 7, by 113% at pH 6, and by 77% at pH 5. Addition of…

MaleLipid PeroxidesThiobarbituric acidIronAscorbic AcidBiochemistryLipid peroxidationchemistry.chemical_compound22'-DipyridylmedicineAnimalsChelationFerrous CompoundsHypoxia BrainAcidosisPharmacologyBrain ChemistryRats Inbred StrainsHydrogen-Ion ConcentrationPhosphateRatsOxygenUltrafiltration (renal)chemistryBiochemistryLipid Peroxidationmedicine.symptomAcidosisAnaerobic exerciseIntracellularBiochemical pharmacology
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Endurance training reduces the susceptibility of mouse skeletal muscle to lipid peroxidation in vitro

1983

Selected estimates of the lipid peroxidative capacity were assayed in the red and white skeletal muscles of control and endurance-trained mice. Endurance training decreased the lipid peroxidation rate in vitro in both muscle types. The concentration of lipids susceptible to Fe2+-induced lipid peroxidation was greater in the red than in the white skeletal muscle and increased after endurance training in the red muscle. Endurance training, however, decreased highly significantly the sensitivity of red muscle to in vitro stimulated lipid peroxidation. The activity of catalase and the concentration of vitamin E were considerably higher in the red muscle, whereas the activity of glutathione pero…

MaleLipid Peroxidesmedicine.medical_specialtyPhysiologymedicine.medical_treatmentMice Inbred StrainsLipid peroxidationMicechemistry.chemical_compoundEndurance trainingInternal medicinemedicineAnimalschemistry.chemical_classificationbiologyChemistryMusclesVitamin EGlutathione peroxidaseSkeletal muscleGlutathioneLipid MetabolismIn vitroEndocrinologymedicine.anatomical_structureCatalasePhysical Endurancebiology.proteinOxidation-ReductionActa Physiologica Scandinavica
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Increased toxicity of cocaine on human hepatocytes induced by ethanol: role of GSH.

1999

Increased toxicity of cocaine to human hepatocytes is observed when cells are simultaneously incubated with ethanol. Ethanol might exacerbate cocaine hepatocyte toxicity by three different pathways: a) by increasing the oxidative metabolism of cocaine and hence the oxidative damage; b) by the formation of a more toxic metabolite, namely cocaethylene; or c) by decreasing the defence mechanisms of the cell (i.e. GSH). In the present study, experiments were conducted to investigate the feasibility of these hypotheses. In hepatocytes preincubated for 48 hr with ethanol, neither significant changes in cocaine metabolism nor cytotoxicity were found despite differences in hepatocyte p-nitrophenol …

MaleLiver cytologyCell SurvivalPharmacologymedicine.disease_causeBiochemistryLipid peroxidationchemistry.chemical_compoundCocaethyleneCocaineDopamine Uptake InhibitorsmedicineHumansCells CulturedAgedGlutathione TransferasePharmacologyEthanolDrug SynergismGlutathioneCYP2E1Middle AgedOxidative Stressmedicine.anatomical_structurechemistryBiochemistryLiverHepatocyteToxicityFemaleOxidative stressmedicine.drugBiochemical pharmacology
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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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