Search results for "mitochondrion"

showing 10 items of 491 documents

Mitochondrial (dys)function - a factor underlying the variability of efavirenz-induced hepatotoxicity?

2015

Background and Purpose The non-nucleoside analogue reverse transcriptase inhibitor efavirenz is associated with hepatic toxicity and metabolic disturbances. Although the mechanisms involved are not clear, recent evidence has pinpointed a specific mitochondrial action of efavirenz accompanied by the induction of an endoplasmic reticulum (ER) stress/unfolded protein response in human hepatic cells. The aim of this study was to further investigate the involvement of this organelle by evaluating efavirenz's effects in cells lacking functional mitochondria (rho°) and comparing them with those of the typical mitotoxic agent rotenone, a standard complex I inhibitor, and the ER stress inducer thaps…

PharmacologyThapsigarginEfavirenzReverse-transcriptase inhibitorEndoplasmic reticulumRotenoneBiologyMitochondrionPharmacologychemistry.chemical_compoundchemistryUnfolded protein responseHepatic stellate cellmedicinemedicine.drugBritish Journal of Pharmacology
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Swelling properties of the mitochondria of unfertilized and newly fertilized sea urchin eggs

1957

Mitocondri isolati da uova vergini e appena fecondate diParacentrotus lividus sono stati trattati con soluzioni di saccarosio a concentrazioni decrescenti, a partire da 0,5M, e con Duponol. Si e trovato che nelle soluzioni ipotoniche il rigonfiamento dei mitocondri e notevolmente maggiore per quelli preparati da uova vergini che per quelli preparati da uova fecondate. Anche al trattamento con Duponol sono piu sensibili i mitocondri delle uova vergini.

PharmacologybiologyZygoteCell BiologyAnatomyMitochondrionMolecular biologyMitochondriaCellular and Molecular NeuroscienceSea Urchinsbiology.animalAnimalsMolecular MedicineMolecular BiologySea urchinExperientia
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Mitochondrial basis of the anti-arrhythmic action of lidocaine and modulation by the n-6 to n-3 PUFA ratio of cardiac phospholipids

2012

The aim of this study was to evaluate the involvement of mitochondria in the mechanism of the anti-arrhythmic lidocaine. Rats were fed with a diet containing either n-6 polyunsaturated fatty acids (PUFAs, SSO group) or an equimolecular mixture of n-3 and n-6 PUFAs (FO group) for 8 weeks. The hearts were perfused according to the working mode using a medium with or without lidocaine 5 μM. They were then subjected to local ischemia (20 min) and reperfusion (30 min). Dietary n-3 PUFAs triggered the expected decrease in the n-6/n-3 PUFA ratio of cardiac phospholipids. Reperfusing the ischemic area favored the incidence of severe arrhythmias. Lidocaine treatment abolished almost completely reper…

Pharmacologychemistry.chemical_classification0303 health sciencesLidocaineLocal anestheticmedicine.drug_classmedicine.medical_treatmentIschemiachemistry.chemical_element030204 cardiovascular system & hematologyCalciumMitochondrionAntiarrhythmic agentPharmacologymedicine.disease03 medical and health sciences0302 clinical medicineAnticonvulsantchemistryAnesthesiamedicinePharmacology (medical)030304 developmental biologyPolyunsaturated fatty acidmedicine.drugFundamental & Clinical Pharmacology
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Zur Wirkung von Butazolidin auf Glutamins�ure-dehydrogenase und ?-Ketoglutarat-oxydase

1957

Glutamic dehydrogenase of rat liver mitochondria is inhibited by phenylbutazone at a final concentration of 2,5 mg-% (0,81 · 10−4 M). However, glutamic dehydrogenase in heart muscle homogenate and the cristalline enzyme from liver are not inhibited by phenylbutazone up to 10 mg-% (3,24 · 10−4 M), but they are inhibited by a metabolite arising during incubation of liver mitochondria with phenylbutazone.

Pharmacologychemistry.chemical_classificationRat liver mitochondriaMetabolitePharmacology toxicologyGeneral MedicineMitochondrionchemistry.chemical_compoundEnzymeBiochemistrychemistryPhenylbutazonemedicineGlutamic dehydrogenaseIncubationmedicine.drugNaunyn-Schmiedebergs Archiv f�r Experimentelle Pathologie und Pharmakologie
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Perspectives and Potential Applications of Mitochondria-Targeted Antioxidants in Cardiometabolic Diseases and Type 2 Diabetes

2013

There is abundant evidence to suggest that mitochondrial dysfunction is a main cause of insulin resistance and related cardiometabolic comorbidities. On the other hand, insulin resistance is one of the main characteristics of type 2 diabetes, obesity, and metabolic syndrome. Lipid and glucose metabolism require mitochondria to generate energy, and when O2 consumption is low due to inefficient nutrient oxidation, there is an increase in reactive oxygen species, which can impair different types of molecules, including DNA, lipids, proteins, and carbohydrates, thereby inducing proinflammatory processes. Factors which contribute to mitochondrial dysfunction, such as mitochondrial biogenesis and…

Pharmacologymedicine.medical_specialtyContext (language use)Type 2 diabetesBiologyMitochondrionBioinformaticsmedicine.diseasemedicine.disease_causeEndocrinologyInsulin resistanceMitochondrial biogenesisDiabetes mellitusInternal medicineDrug DiscoverymedicineMolecular MedicineMetabolic syndromeOxidative stressMedicinal Research Reviews
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Molecular Mechanisms of the Crosstalk Between Mitochondria and NADPH Oxidase Through Reactive Oxygen Species—Studies in White Blood Cells and in Anim…

2014

Aims: Oxidative stress is involved in the development of cardiovascular disease. There is a growing body of evidence for a crosstalk between different enzymatic sources of oxidative stress. With the present study, we sought to determine the underlying crosstalk mechanisms, the role of the mitochondrial permeability transition pore (mPTP), and its link to endothelial dysfunction. Results: NADPH oxidase (Nox) activation (oxidative burst and translocation of cytosolic Nox subunits) was observed in response to mitochondrial reactive oxygen species (mtROS) formation in human leukocytes. In vitro, mtROS-induced Nox activation was prevented by inhibitors of the mPTP, protein kinase C, tyrosine kin…

PhysiologyNeutrophilsClinical BiochemistryBiologyMitochondrionmedicine.disease_causeBiochemistryModels BiologicalSuperoxide dismutaseCyclophilinsMiceForum Original Research CommunicationsMitochondria (A. Daiber Ed.)medicineLeukocytesAnimalsHumansMolecular BiologyGeneral Environmental ScienceRespiratory Burstchemistry.chemical_classificationMice KnockoutReactive oxygen speciesNADPH oxidaseSuperoxide DismutaseAngiotensin IINADPH OxidasesBiological TransportCell BiologyRespiratory burstMitochondriaPeroxidesEnzyme ActivationCrosstalk (biology)Oxidative StressMitochondrial permeability transition poreBiochemistrychemistrybiology.proteincardiovascular systemGeneral Earth and Planetary SciencesReactive Oxygen SpeciesOxidation-ReductionOxidative stressCyclophilin D
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ATP distribution and localization of mitochondria in Suberites domuncula (Olivi 1792) tissue

2011

SUMMARY The metabolic energy state of sponge tissue in vivo is largely unknown. Quantitative bioluminescence-based imaging was used to analyze the ATP distribution of Suberites domuncula (Olivi 1792) tissue, in relation to differences between the cortex and the medulla. This method provides a quantitative picture of the ATP distribution closely reflecting the in vivo situation. The obtained data suggest that the highest ATP content occurs around channels in the sponge medulla. HPLC reverse-phase C-18, used for measurement of ATP content, established a value of 1.62 μmol ATP g–1 dry mass in sponge medulla, as opposed to 0.04 μmol ATP g–1 dry mass in the cortex, thus indicating a specific and…

PhysiologyProtein subunitIn situ hybridizationAquatic ScienceBiologyMitochondrionAdenosine TriphosphateImage Processing Computer-AssistedAnimalsMolecular BiologyChromatography High Pressure LiquidIn Situ HybridizationEcology Evolution Behavior and SystematicsMedullaArginine KinaseArginine kinaseATP distribution; mitochondria; imaging bioluminescence; HPLC; Porifera; Suberites domunculabiology.organism_classificationImmunohistochemistryMitochondriaSuberites domunculaSpongeBiochemistryOrgan SpecificityInsect Sciencebiology.proteinAnimal Science and ZoologyMitochondrion localizationEnergy MetabolismSuberitesJournal of Experimental Biology
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What is the function of neuroglobin?

2009

SUMMARY For a long time, haemoglobin and myoglobin had been assumed to represent the only globin types of vertebrates. In 2000, however, we discovered a third globin type by mining the genome sequence data. Based on a preferential expression in the nervous system, this globin is referred to as neuroglobin. Despite nine years of research, its function is still uncertain and a number of hypotheses have been put forward. Neuroglobin enhances cell viability under hypoxia and under various types of oxidative stress in transgenic systems, but does not appear to be strongly upregulated in response to stress. A close phylogenetic relationship with invertebrate nerve globins and its positive correla…

PhysiologyTransgeneCellNeuroglobinNerve Tissue ProteinsAquatic ScienceMitochondrionBiologymedicine.disease_causeNervous Systemchemistry.chemical_compoundmedicineAnimalsGlobinHypoxiaMolecular BiologyEcology Evolution Behavior and SystematicsReactive nitrogen speciesNeuronsCytoglobinReactive Nitrogen SpeciesCell biologyGlobinsOxygenmedicine.anatomical_structurechemistryBiochemistryGene Expression RegulationInsect ScienceNeuroglobinVertebratesAnimal Science and ZoologyReactive Oxygen SpeciesOxidative stressThe Journal of experimental biology
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Amorphous Ca2+ polyphosphate nanoparticles regulate the ATP level in bone-like SaOS-2 cells

2015

ABSTRACT Polyphosphate (polyP) is a physiologically occurring polyanion that is synthesized especially in bone-forming osteoblast cells and blood platelets. We used amorphous polyP nanoparticles, complexed with Ca2+, that have a globular size of ∼100 nm. Because polyP comprises inorganic orthophosphate units that are linked together through high-energy phosphoanhydride bonds, we questioned whether the observed morphogenetic effect, elicited by polyP, is correlated with the energy-generating machinery within the cells. We show that exposure of SaOS-2 osteoblast-like cells to polyP results in a strong accumulation of mitochondria and a parallel translocation of the polyP-degrading enzyme alka…

PolyphosphateOsteoblastCell BiologyBiologyMitochondrionAscorbic aciddigestive system diseaseschemistry.chemical_compoundmedicine.anatomical_structurechemistryBiochemistryotorhinolaryngologic diseasesBiophysicsExtracellularmedicineAlkaline phosphataseSaos-2 cellsIntracellularJournal of Cell Science
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Oxidative stress and mitochondrial dysfunction in Kindler syndrome

2014

This is an Open Access article distributed under the terms of the Creative Commons Attribution License.-- et al.

Premature agingMaleKeratinocytesAdolescentComputingMilieux_LEGALASPECTSOFCOMPUTINGMitochondrionmedicine.disease_causePathogenesisKindler syndrome03 medical and health scienceschemistry.chemical_compound0302 clinical medicineBlistermedicineHumansGenetics(clinical)Pharmacology (medical)Photosensitivity DisordersGenodermatosisChildGenetics (clinical)Cells CulturedPeriodontal Diseases030304 developmental biologyAged 80 and overMedicine(all)0303 health sciencesintegumentary systemResearchGeneral MedicineGlutathioneMiddle Agedmedicine.diseaseMalondialdehydeMolecular biology3. Good healthMitochondriaOxidative StresschemistryOxidative stress030220 oncology & carcinogenesisChild PreschoolFemaleSkin cancerEpidermolysis BullosaKindlin1Oxidative stressOrphanet Journal of Rare Diseases
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