Search results for "Membrane potential"

showing 7 items of 327 documents

Model-specific effects of bumetanide on epileptiform activity in the in-vitro intact hippocampus of the newborn mouse.

2007

The immature brain has a higher susceptibility to develop seizures, which often respond poorly to classical pharmacological treatment. It has been recently suggested that bumetanide, which blocks Na(+)-dependent K(+)-Cl(-)-cotransporter isoform 1 (NKCC1) and thus attenuates depolarizing GABAergic responses, could soothe epileptiform activity in immature nervous systems. To evaluate whether bumetanide consistently attenuates epileptiform activity, we investigated the effect of 10 microM bumetanide in five different in-vitro epilepsy models using field potential recordings in the CA3 region of intact mouse hippocampal preparations at postnatal day 4-7. Bumetanide reduced amplitude and frequen…

medicine.medical_specialtySodium-Potassium-Chloride SymportersHippocampusKainate receptorHippocampal formationIn Vitro TechniquesHippocampusMembrane PotentialsCellular and Molecular Neurosciencechemistry.chemical_compoundEpilepsyMiceChloride ChannelsInternal medicinemedicineAnimalsSolute Carrier Family 12 Member 2MagnesiumBumetanidePharmacologyEpilepsyDepolarizationStrychninemedicine.diseaseDisease Models AnimalEndocrinologychemistryAnimals NewbornGabazinePotassiumBumetanidemedicine.drugNeuropharmacology
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Oxygen and substrate deprivation on isolated rat cardiac myocytes : temporal relationship between electromechanical and biochemical consequences

1990

The effects of hypoxia and reoxygenation on action potentials (AP), contractions, and certain biochemical parameters were studied in isolated rat ventricular myocytes in monolayer culture in the presence and absence of glucose. Substrate deprivation alone had no influence on the basal properties. In the presence of glucose, a 4-h hypoxic treatment caused only a moderate decrease in AP amplitude and rate. In substrate-free conditions, hypoxia induced a gradual decline in plateau potential level and in AP duration and rate, followed by rhythm abnormalities and a failure of the electromechanical coupling. Spontaneous AP generation then ceased, and the resting potential decreased with increase…

medicine.medical_specialtyTime FactorsPhysiology[SDV]Life Sciences [q-bio]Action Potentialschemistry.chemical_element030204 cardiovascular system & hematologyBiologyGLYCOSEACIDE LACTIQUEOxygenMembrane PotentialsContractility03 medical and health sciencesAdenosine Triphosphate0302 clinical medicinePhysiology (medical)Internal medicinemedicineAnimalsMyocyteHypoxiaCells Cultured030304 developmental biologyPharmacologyFREQUENCE0303 health sciencesL-Lactate DehydrogenaseMyocardiumRats Inbred StrainsBiological activityGeneral MedicineHypoxia (medical)Myocardial ContractionRatsElectrophysiologyATP[SDV] Life Sciences [q-bio]ElectrophysiologyGlucoseEndocrinologychemistryCell cultureCirculatory systemLactatesBiophysicsRATmedicine.symptom
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Mitochondrial complex I impairment in leukocytes from polycystic ovary syndrome patients with insulin resistance.

2009

Insulin resistance is a feature of polycystic ovary syndrome (PCOS) and is related to mitochondrial function.Our objective was to assess mitochondrial function by evaluating mitochondrial oxygen (O(2)) consumption, reactive oxygen species (ROS) production, levels of glutathione (GSH), the oxidized glutathione/GSH ratio, TNFalpha levels, and membrane potential. Additionally, we have evaluated mitochondrial complex I as a target of the oxidative stress responsible for PCOS in polymorphonuclear cells.This was a prospective controlled study conducted in an academic medical center.The study population consisted of 20 lean reproductive-age women with PCOS and 20 body composition-matched controls.…

medicine.medical_specialtyendocrine system diseasesEndocrinology Diabetes and Metabolismmedicine.medical_treatmentClinical BiochemistryContext (language use)BiologyMitochondrionmedicine.disease_causeBiochemistrychemistry.chemical_compoundEndocrinologyInsulin resistanceOxygen ConsumptionInternal medicinemedicineLeukocytesHumanschemistry.chemical_classificationMembrane Potential MitochondrialReactive oxygen speciesElectron Transport Complex ITumor Necrosis Factor-alphaInsulinBiochemistry (medical)nutritional and metabolic diseasesGlutathionemedicine.diseasePolycystic ovaryGlutathionefemale genital diseases and pregnancy complicationsEndocrinologychemistryFemaleInsulin ResistanceReactive Oxygen SpeciesOxidative stressPolycystic Ovary Syndrome
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Mechanisms of cell death in canine parvovirus-infected cells provide intuitive insights to developing nanotools for medicine

2010

Jonna Nykky, Jenni E Tuusa, Sanna Kirjavainen, Matti Vuento, Leona GilbertNanoscience Center and Department of Biological and Environmental Science, University of Jyväskylä, FinlandAbstract: Viruses have great potential as nanotools in medicine for gene transfer, targeted gene delivery, and oncolytic cancer virotherapy. Here we have studied cell death mechanisms of canine parvovirus (CPV) to increase the knowledge on the CPV life cycle in order to facilitate the development of better parvovirus vectors. Morphological studies of CPV-infected Norden laboratory feline kidney (NLFK) cells and canine fibroma cells (A72) displayed characteristic apoptotic events. Apoptosis was f…

nekroosianimal diseasesvirusesGene ExpressionPharmaceutical ScienceApoptosisViral Nonstructural Proteinsnecrosis0302 clinical medicineInternational Journal of NanomedicineDrug DiscoveryCaspaseOriginal ResearchMembrane Potential MitochondrialOncolytic Virotherapy0303 health sciencesCell DeathbiologynanoparticleCell Cycleapoptosiscanine parvovirusCanine parvovirusGeneral MedicineFlow Cytometry3. Good healthNanomedicineCaspases030220 oncology & carcinogenesisvirotherapyProgrammed cell deathParvovirus CaninenanopartikkeliBiophysicsBioengineeringDNA FragmentationGene deliveryCell LineBiomaterials03 medical and health sciencesDogsMicroscopy Electron TransmissionAnimalsHumansVirotherapyapoptoosi030304 developmental biologyParvovirusOrganic Chemistrybiology.organism_classificationVirologyOncolytic viruskoiran parvovirusviroterapiaMicroscopy FluorescenceApoptosisCatsbiology.proteinDNA DamageHeLa CellsInternational Journal of Nanomedicine
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In Vitro Cytotoxic Effect of Aqueous Extracts from Leaves and Rhizomes of the Seagrass Posidonia oceanica (L.) Delile on HepG2 Liver Cancer Cells: Fo…

2023

Aqueous extracts from Posidonia oceanica’s green and brown (beached) leaves and rhizomes were prepared, submitted to phenolic compound and proteomic analysis, and examined for their potential cytotoxic effect on HepG2 liver cancer cells in culture. The chosen endpoints related to survival and death were cell viability and locomotory behavior, cell-cycle analysis, apoptosis and autophagy, mitochondrial membrane polarization, and cell redox state. Here, we show that 24 h exposure to both green-leaf- and rhizome-derived extracts decreased tumor cell number in a dose–response manner, with a mean half maximal inhibitory concentration (IC50) estimated at 83 and 11.5 μg of dry extract/mL, respecti…

phenolic compoundreactive oxygen specieSettore CHIM/10 - Chimica Degli AlimentiGeneral Immunology and MicrobiologycaspaseSettore BIO/05 - Zoologiaproteomic analysiscell biology; cell cycle; reactive oxygen species; wound healing assay; caspases; mitochondrial transmembrane potential; clonogenic assay; phenolic compounds; proteomic analysisGeneral Biochemistry Genetics and Molecular Biologycell biologymitochondrial transmembrane potentialcell cycleclonogenic assaySettore BIO/06 - Anatomia Comparata E CitologiaGeneral Agricultural and Biological Scienceswound healing assayBiology
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Aplidin® induces JNK-dependent apoptosis in human breast cancer cells via alteration of glutathione homeostasis, Rac1 GTPase activation, and MKP-1 ph…

2006

Aplidin® is an antitumor agent in phase II clinical trials that induces apoptosis through the sustained activation of Jun N-terminal kinase (JNK). We report that Aplidin® alters glutathione homeostasis increasing the ratio of oxidized to reduced forms (GSSG/GSH). Aplidin® generates reactive oxygen species and disrupts the mitochondrial membrane potential. Exogenous GSH inhibits these effects and also JNK activation and cell death. We found two mechanisms by which Aplidin® activates JNK: rapid activation of Rac1 small GTPase and downregulation of MKP-1 phosphatase. Rac1 activation was diminished by GSH and enhanced by L-buthionine (SR)-sulfoximine, which inhibits GSH synthesis. Downregulatio…

rac1 GTP-Binding ProteinProgrammed cell deathSmall interfering RNAGlutathione reductaseDown-RegulationAntineoplastic AgentsApoptosisBreast NeoplasmsCell Cycle ProteinsBiologyPeptides CyclicImmediate-Early ProteinsMembrane Potentialschemistry.chemical_compoundMiceDownregulation and upregulationDepsipeptidesProtein Phosphatase 1Phosphoprotein PhosphatasesAnimalsHomeostasisHumansMolecular Biologychemistry.chemical_classificationReactive oxygen speciesGlutathione PeroxidaseGlutathione DisulfideJNK Mitogen-Activated Protein KinasesProtein phosphatase 1Dual Specificity Phosphatase 1Cell BiologyGlutathioneCell biologyEnzyme ActivationOxidative StressGlutathione ReductasechemistryMitochondrial MembranesGlutathione disulfideCalciumProtein Tyrosine PhosphatasesReactive Oxygen SpeciesCopperHeLa CellsCell Death and Differentiation
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Biological and Proteomic Characterization of the Anti-Cancer Potency of Aqueous Extracts from Cell-Free Coelomic Fluid of Arbacia lixula Sea Urchin i…

2022

Echinoderms are an acknowledged source of bioactive compounds exerting various beneficial effects on human health. Here, we examined the potential in vitro anti-hepatocarcinoma effects of aqueous extracts of the cell-free coelomic fluid obtained from the sea urchin Arbacia lixula using the HepG2 cell line as a model system. This was accomplished by employing a combination of colorimetric, microscopic and flow cytometric assays to determine cell viability, cell cycle distribution, the possible onset of apoptosis, the accumulation rate of acidic vesicular organelles, mitochondrial polarization, cell redox state and cell locomotory ability. The obtained data show that exposed HepG2 cells under…

reactive oxygen specieSettore CHIM/10 - Chimica Degli AlimentiSettore BIO/05 - ZoologiaHepG2 cellOcean Engineeringapoptosisea urchinechinodermmitochondrial transmembrane potentialcell cycleacidic vesicular organelleSettore BIO/06 - Anatomia Comparata E Citologiacoelomic fluidcoelomic fluid; sea urchin; echinoderm; HepG2 cells; apoptosis; cell cycle; acidic vesicular organelles; mitochondrial transmembrane potential; reactive oxygen species; wound healing assaywound healing assayWater Science and TechnologyCivil and Structural EngineeringJournal of Marine Science and Engineering
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