Search results for "Cell damage"

showing 10 items of 38 documents

Effects of tributyltin(IV) chloride on the gametes and fertilization ofAscidia malaca (Ascidiacea: Tunicata)

2003

Ascidia malaca gametes before fertilization incubated in 10-5 or 10-7 M solutions of tributyltin(IV) chloride, TBTCl, for 3 h appear highly damaged under transmission electron microscopy observation. Also, the fertilization process is affected by the compound: the damaged spermatozoa are present in the vitelline coat and the egg does not cleave. An increase of microbodies, structurally similar to peroxisomes, have been detected in the egg peripheral cytoplasm, probably in relation to their role in alleviating damage to some cellular components. The results have shown that the reproduction of ascidians under unfavourable environmental conditions is prevented. Copyright © 2003 John Wiley &amp…

Ascidianmedia_common.quotation_subjectgameteanimal cellChloridereproductionInorganic Chemistrychemistry.chemical_compoundGametes and reproductionHuman fertilizationenvironmental factortransmission electron microscopymedicinetributyltin chlorideMicrobodycontrolled studyperoxisomevitelline membranemedia_commonAscidiaceanonhumanbiologyChemistryPeroxisomes proliferationarticleGeneral Chemistrybiology.organism_classificationCell biologycell damagemicrobodyAscidiamedicine.anatomical_structurespermatozoonTributyltin(IV) chlorideChemistry (miscellaneous)fertilizationSettore CHIM/03 - Chimica Generale E InorganicacytoplasmTributyltinGameteoocyte cleavageReproductionAscidiaceacell structuremedicine.drugApplied Organometallic Chemistry
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The MDM2-p53 pathway is involved in preconditioning-induced neuronal tolerance to ischemia

2018

Brain preconditioning (PC) refers to a state of transient tolerance against a lethal insult that can be evoked by a prior mild event. It is thought that PC may induce different pathways responsible for neuroprotection, which may involve the attenuation of cell damage pathways, including the apoptotic cell death. In this context, p53 is a stress sensor that accumulates during brain ischemia leading to neuronal death. The murine double minute 2 gene (MDM2), a p53-specific E3 ubiquitin ligase, is the main cellular antagonist of p53, mediating its degradation by the proteasome. Here, we study the role of MDM2-p53 pathway on PC-induced neuroprotection both in cultured neurons (in vitro) and rat …

Cell death0301 basic medicineProgrammed cell deathCell SurvivalNeuronalScience2415 Biología MolecularIschemiaNeuroprotectionArticleBrain ischemiaMiceBrain ischemia03 medical and health sciences0302 clinical medicineIschemiaXarxes neuronals (Neurobiologia)medicineAnimalsIschemic PreconditioningCell damageCells CulturedBrain preconditioningNeuronsMultidisciplinarybiologyChemistryQRBrainProto-Oncogene Proteins c-mdm2MDM2-p53medicine.diseaseNeuroprotectionRatsCell biologyUbiquitin ligaseDisease Models Animal030104 developmental biology2490 Neurocienciasbiology.proteinMedicineIschemic preconditioningMdm2Tumor Suppressor Protein p53030217 neurology & neurosurgerySignal Transduction
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Interplay of oxidants and antioxidants during exercise: Implications for muscle health

2010

Muscle contraction results in generation of reactive oxygen and nitrogen species (RONS) at a rate determined by the intensity, frequency, and duration of the exercise protocols. Strenuous exercise causes oxidation of protein, lipid, and DNA, release of cytosolic enzymes, and other signs of cell damage; however, only exhaustive exercise is detrimental. Indeed, the regulation of vascular tone, the excitation-contraction coupling, growth, and differentiation in skeletal muscle, are governed in part by RONS. This is accomplished by RONS interaction with redox-sensitive transcription factors, leading to increased gene expression of antioxidant enzymes, cytoprotective proteins, and other enzymes …

Cell signalingmedicine.medical_specialtyFree RadicalsHealth StatusGene ExpressionPhysical Therapy Sports Therapy and Rehabilitationmedicine.disease_causeAntioxidantsInternal medicinemedicineHumansOrthopedics and Sports MedicineExercise physiologyMuscle SkeletalExerciseTranscription factorCell damageExercise ToleranceChemistryNF-kappa BSkeletal musclemedicine.diseaseAdaptation PhysiologicalReactive Nitrogen SpeciesOxidative Stressmedicine.anatomical_structureEndocrinologyMitogen-Activated Protein KinasesSignal transductionmedicine.symptomReactive Oxygen SpeciesOxidation-ReductionOxidative stressMuscle ContractionSignal TransductionMuscle contraction
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MOLECULAR BASIS OF DRUG PHOTOTOXICITY: PHOTOSENSITIZED CELL DAMAGE BY THE MAJOR PHOTOPRODUCT OF TIAPROFENIC ACID

1994

Tiaprofenic acid is a photosensitizing nonsteroidal anti-inflammatory drug, whose major photoproduct (decarboxytiaprofenic acid) is also a potent photosensitizer. Because of the lack of the carboxylate moiety, this photoproduct is more lipophilic and might bind more efficiently to cell membranes, thereby causing phototoxic damage. To verify the feasibility of this hypothesis, we have prepared the 3H-labeled analogs of tiaprofenic acid and its photoproduct and examined the binding, persistence and phototoxicity of the photoproduct using poorly metabolizing (fibroblasts) and actively metabolizing cells (hepatocytes). The photoproduct of tiaprofenic acid accumulates in both cell types as it is…

Cell typePhotochemistryCellBiochemistryIn vivomedicineHumansPhotosensitizerPhysical and Theoretical ChemistryCell damageCells CulturedBinding SitesPhotosensitizing AgentsChemistryGeneral MedicineFibroblastsmedicine.diseasePhotobleachingmedicine.anatomical_structureBiochemistrybiological sciencessense organsPropionatesPhototoxicityTiaprofenic acidmedicine.drugPhotochemistry and Photobiology
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Ozone-induced reductions in below-ground biomass: an anatomical approach in potato

2010

[EN] Potato plants were grown in open-top chambers under three ozone concentrations during two complete cropping seasons (93 and 77 d in 2004 and 2005, respectively). The effects of chronic exposure to ozone on leaf anatomy, cell ultrastructure and crop yield were studied. Severe cell damage was found, even at ambient ozone levels, mainly affecting the spongy parenchyma and areas near the stomata. Damage to the cell wall caused loss of cell contact, and loss of turgor pressure due to tonoplast disintegration, contributed to cell collapse. Phloem sieve plates were obstructed by callose accumulation, and damaged mesophyll cells increased their starch stores. Tuber yield fell sharply (24–44%),…

Crops AgriculturalOzonePhysiologyStarchTurgor pressureBOTANICABiomassPlant ScienceBiologyopen-top chamberschemistry.chemical_compoundAir PollutionmedicineBiomassassimilate partitioningCell damageSolanum tuberosumBIOLOGIA VEGETALCalloseCrop yieldfungiCallosefood and beveragesStarchcrop yieldmedicine.diseasePlant LeavesPlant TubersozonechemistryAgronomypotatoleaf anatomyPhloem
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2019

From the very beginnings of radiotherapy, a crucial question persists with how to target the radiation effectiveness into the tumor while preserving surrounding tissues as undamaged as possible. One promising approach is to selectively pre-sensitize tumor cells by metallic nanoparticles. However, though the “physics” behind nanoparticle-mediated radio-interaction has been well elaborated, practical applications in medicine remain challenging and often disappointing because of limited knowledge on biological mechanisms leading to cell damage enhancement and eventually cell death. In the present study, we analyzed the influence of different nanoparticle materials (platinum (Pt), and gold (Au)…

DNA damageDNA repairNanoparticle02 engineering and technologyCatalysislaw.inventionIonizing radiationInorganic Chemistry03 medical and health sciences0302 clinical medicineConfocal microscopylawmedicinePhysical and Theoretical ChemistryMolecular BiologyCell damageSpectroscopySuper-resolution microscopyOrganic ChemistryGeneral Medicine021001 nanoscience & nanotechnologymedicine.disease3. Good healthComputer Science Applications030220 oncology & carcinogenesisCancer cellBiophysics0210 nano-technologyInternational Journal of Molecular Sciences
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The impact of dehydration rate on the production and cellular location of reactive oxygen species in an aquatic moss.

2012

† Background and Aims The aquatic moss Fontinalis antipyretica requires a slow rate of dehydration to survive a desiccation event. The present work examined whether differences in the dehydration rate resulted in corresponding differences in the production of reactive oxygen species (ROS) and therefore in the amount of cell damage. † Methods Intracellular ROS production by the aquatic moss was assessed with confocal laser microscopy and the ROS-specific chemical probe 2,7-dichlorodihydrofluorescein diacetate. The production of hydrogen peroxide was also quantified and its cellular location was assessed. † Key Results The rehydration of slowly dried cells was associated with lower ROS produc…

Fontinalis antipyreticaTime FactorsCell Survivalved/biology.organism_classification_rank.specieschemistry.chemical_elementPlant ScienceBiologyOxygenchemistry.chemical_compoundmedicineDehydrationDesiccationHydrogen peroxideCell damagechemistry.chemical_classificationReactive oxygen speciesMicroscopy ConfocalDehydrationved/biologyHydrogen PeroxideOriginal Articlesmedicine.diseaseBryopsidaRespiratory burstOxygenPlant LeavesOxidative StresschemistryBiochemistryBiophysicsReactive Oxygen SpeciesIntracellularAnnals of botany
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Impact of therapeutically induced reactive oxygen species and radical scavenging by α-tocopherol on tumor cell adhesion

2007

Many tumor treatment modalities such as ionizing radiation or some chemotherapy induce reactive oxygen species (ROS) resulting in therapeutic cell damage. The aim of this study was to analyze whether such ROS induction may affect the mechanical stability of solid tumor tissue by degradation of the extracellular matrix proteins or by a loss of cell adhesion molecules. Additionally, the protective impact of alpha-tocopherol treatment on these processes was studied. Experimental DS-sarcomas in rats were treated with a combination of localized 44 degrees C hyperthermia, inspiratory hyperoxia and xanthine oxidase in order to induce pronounced oxidative stress. A second group of animals were pret…

Hyperoxiachemistry.chemical_classificationCancer ResearchReactive oxygen speciesbiologyCell adhesion moleculeIntegrinGeneral Medicinemedicine.diseasemedicine.disease_causeExtracellular matrixchemistry.chemical_compoundOncologyBiochemistrychemistrymedicinebiology.proteinCancer researchmedicine.symptomXanthine oxidaseCell damageOxidative stressOncology Reports
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Host–pathogen interactions in Vibrio vulnificus: responses of monocytes and vascular endothelial cells to live bacteria

2015

ABSTRACT  Aim: To demonstrate that Vibrio vulnificus, a sepsis-related aquatic pathogen, can provoke a strong pro-inflammatory reaction in blood-associated target cells. Materials & methods: We selected two strains of the two main phylogenetic lineages, two human cell lines, monocytes and vascular endothelial cells and designed an in vitro infection model simulating early septicemia. Results: Both strains caused a strong cell-specific pro-inflammatory response and produced a high degree of cell damage that ended with death by lysis (endothelial cells) or apoptosis/lysis (monocytes). The interaction with endothelial cells was stronger than expected and significantly different for both l…

InflammationMicrobiology (medical)LysisbiologyGene Expression ProfilingEndothelial CellsVibrio vulnificusbiology.organism_classificationmedicine.diseaseMicrobiologyVirologyMonocytesIn vitroMicrobiologySepsisStress PhysiologicalApoptosisHost-Pathogen InteractionsmedicineHumansVibrio vulnificusPathogenCell damageCells CulturedBacteriaFuture Microbiology
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Pathophysiology of traumatic brain injury.

2007

The knowledge of the pathophysiology after traumatic head injury is necessary for adequate and patient-oriented treatment. As the primary insult, which represents the direct mechanical damage, cannot be therapeutically influenced, target of the treatment is the limitation of the secondary damage (delayed non-mechanical damage). It is influenced by changes in cerebral blood flow (hypo- and hyperperfusion), impairment of cerebrovascular autoregulation, cerebral metabolic dysfunction and inadequate cerebral oxygenation. Furthermore, excitotoxic cell damage and inflammation may lead to apoptotic and necrotic cell death. Understanding the multidimensional cascade of secondary brain injury offers…

InflammationNecrosisTraumatic brain injurybusiness.industryInflammationVasospasmBrain Edemamedicine.disease_causemedicine.diseaseBioinformaticsPathophysiologyOxidative StressAnesthesiology and Pain MedicineOxygen ConsumptionCerebral blood flowAnesthesiaBrain InjuriesCerebrovascular CirculationmedicineHumansmedicine.symptombusinessCell damageOxidative stressBritish journal of anaesthesia
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