Search results for "DNA laddering"

showing 4 items of 4 documents

Pregnenolone sulfate, a naturally occurring excitotoxin involved in delayed retinal cell death.

2002

The present study was designed to investigate the neurosteroid pregnenolone sulfate (PS), known for its ability to modulate NMDA receptors and interfere with acute excitotoxicity, in delayed retinal cell death. Three hours after exposure of the isolated and intact retina to a 30-min PS pulse, DNA fragmentation as assessed by genomic DNA gel electrophoresis and a modified in situ terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end-labeling (TUNEL) method appeared concurrently with an increase in superoxide dismutase (SOD) activity and thiobarbituric acid-reactive substances (TBARS) levels. At 7 h, the increased amount of DNA laddering was accompanied by a higher number of TUN…

Malemedicine.medical_specialtyNeurotoxinsExcitotoxicityApoptosisDNA FragmentationDNA ladderingBiologymedicine.disease_causeBiochemistryReceptors N-Methyl-D-AspartateThiobarbituric Acid Reactive SubstancesRetinaCellular and Molecular Neurosciencechemistry.chemical_compoundAdjuvants ImmunologicSuperoxidesInternal medicinemedicineTBARSIn Situ Nick-End LabelingAnimalsCycloheximideRats WistarProgesteroneProtein Synthesis InhibitorsTUNEL assayEstradiolL-Lactate DehydrogenaseDehydroepiandrosterone SulfateSuperoxide DismutaseRatsEndocrinologychemistryApoptosisPregnenolonePregnenoloneDNA fragmentationLipid PeroxidationPregnenolone sulfateReactive Oxygen Speciesmedicine.drugJournal of neurochemistry
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2005

Ethanol inhibits proliferation in astrocytes, an effect that was recently linked to the suppression of phosphatidic acid (PA) formation by phospholipase D (PLD). The present study investigates ethanol's effect on the induction of apoptosis in astrocytes and the formation of ceramide, an apoptotic signal. Evidence is presented that the formation of PA and ceramide may be reciprocally linked during ethanol exposure. In cultured rat cortical astrocytes, ethanol (0.3–1 %, v/v) induced nuclear fragmentation and DNA laddering indicative of apoptosis. Concomitantly, in cells prelabeled with [3H]-serine, ethanol caused a dose-dependent, biphasic increase of the [3H]-ceramide/ [3H]-sphingomyelin rat…

PharmacologyCeramidePhospholipase DLipid signalingPhosphatidic acidDNA ladderingBiologyCell biologychemistry.chemical_compoundchemistryApoptosisPharmacology (medical)Fragmentation (cell biology)SphingomyelinBMC Pharmacology
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Apoptotic effects of different drugs on cultured retinoblastoma Y79 cells

1998

This paper deals with the apoptotic effect exerted in human retinoblastoma Y79 cells by a number of compounds. A remarkable effect was observed after treatment with DNA-damaging agents, such as camptothecin, etoposide, cisplatin and carboplatin; camptothecin was found to be the most efficacious. Treatment with these compounds induced the appearance of morphological features of apoptosis in the cells together with the distinct fragmentation of DNA, as shown by agarose gel electrophoresis. These effects were also accompanied by a remarkable increase in the level of p53. Many other compounds, which are not DNA-damaging agents, induced the morphological features of apoptosis but none of them we…

AmsacrinePaclitaxelDNA damageAntineoplastic AgentsApoptosisSuraminDNA ladderingBiologyretinoblastomaCarboplatinchemistry.chemical_compoundTumor Cells CulturedmedicineHumansFragmentation (cell biology)EtoposideCisplatinSodium butyrateGeneral MedicineAntineoplastic Agents PhytogenicMolecular biologyButyrateschemistryApoptosisAgarose gel electrophoresisImmunologyButyric AcidCamptothecinCisplatinDrug Screening Assays AntitumorCamptothecinDNA Damagemedicine.drug
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Calcitonin gene-related peptide partly protects cultured smooth muscle cells from apoptosis induced by an oxidative stress via activation of ERK1/2 M…

2003

Abstract Oxidative stress induced by a glucose/glucose oxidase (G/GO) generator system dose-dependently decreased the viability of cultured vascular smooth muscle cells (VSMC) as estimated by MTT assay. Cell death was induced in 40% of cells exposed to 0.2 IU/ml of the free radical generating mixture. Annexin-V labeling, Hoechst staining together with DNA laddering demonstrated that apoptosis was responsible for this cell loss. Pretreatment of the cells with 10−8 M calcitonin gene-related peptide (CGRP) significantly attenuated the damaging effect of the oxidative stress. Indeed, cell viability was estimated to be 80% in CGRP-treated group, instead of 60% in absence of CGRP treatment. This …

Programmed cell deathVascular smooth musclep38 mitogen-activated protein kinasesCalcitonin Gene-Related PeptideMyocytes Smooth MuscleApoptosisBiologyDNA ladderingCalcitonin gene-related peptidemedicine.disease_causeProtective AgentsMuscle Smooth VascularmedicineAnimalsHumansCGRPViability assayRats WistarMolecular BiologyCells CulturedMitogen-Activated Protein Kinase 3integumentary systemSAPKCell BiologyHydrogen PeroxideMAPKMolecular biologyRatsUp-RegulationNeuropeptideOxidative StressMitogen-activated protein kinaseVascular smooth muscle cellbiology.proteinMitogen-Activated Protein KinasesOxidative stressReceptors Calcitonin Gene-Related PeptideSignal TransductionBiochimica et biophysica acta
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