Search results for "MITO"

showing 10 items of 2513 documents

Late onset administration of oral antioxidants prevents age-related loss of motor co-ordination and brain mitochondrial DNA damage.

1999

We have studied the effect of aging on brain glutathione redox ratio, on brain mitochondrial DNA damage and on motor co-ordination in mice and the possible protective role of late onset administration of sulphur-containing antioxidants. Glutathione redox ratios change to a more oxidized state in whole brain with aging but the changes are much more pronounced when this ratio is measured in brain mitochondria. The levels of 8-oxo-7,8-dihydro-2 '-deoxyguanosine in mitochondrial DNA are much higher in the brain of old animals than in those of young ones. Late onset oral administration of sulphur-containing antioxidants partially prevents oxidation of mitochondrial glutathione and DNA. There is …

Malemedicine.medical_specialtyMitochondrial DNAAgingAdministration OralLate onsetMice Inbred StrainsBiologyMotor Activitymedicine.disease_causeBiochemistryRedoxDNA MitochondrialAntioxidantsDrug Administration Schedulechemistry.chemical_compoundMiceOral administrationInternal medicineAge relatedmedicineAnimalsPostural BalanceAlanineBrainDeoxyguanosineGeneral MedicineGlutathioneMolecular biologyGlutathioneThiazolesEndocrinologychemistry8-Hydroxy-2'-DeoxyguanosineOxidation-ReductionOxidative stressDNASulfurDNA DamageFree radical research
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Mitochondrial glutathione oxidation correlates with age-associated oxidative damage to mitochondrial DNA

1996

Mitochondria may be primary targets of free radical damage associated with aging. We have found that mitochondrial glutathione is markedly oxidized with aging in rats and mice. The oxidized to reduced glutathione ratio rises with aging in the liver, kidney, and brain. The magnitude of these changes is much higher than that previously found in whole cells of any species previously studied. In the liver, this ratio (expressing GSSG as a percent of GSH) changed from 0.77 +/- 0.19% (n=5) in young rats to 2.47 +/- 1.25% (n=5) in old ones, i.e., 320% of the controls. In the brain and kidney, values for old rats were, respectively, 600 and 540% higher than those of young rats. A marked oxidation o…

Malemedicine.medical_specialtyMitochondrial DNAAgingAntioxidantmedicine.medical_treatmentMitochondrionmedicine.disease_causeBiochemistryDNA MitochondrialAntioxidantschemistry.chemical_compoundMiceInternal medicineGeneticsmedicineDeoxyguanosineAnimalsRats WistarMolecular BiologyFree-radical theory of agingKidneyGlutathione DisulfideChemistryDeoxyguanosineGlutathioneGlutathioneRatsMice Inbred C57BLOxidative StressEndocrinologymedicine.anatomical_structure8-Hydroxy-2'-DeoxyguanosineRabbitsOxidation-ReductionOxidative stressBiotechnologyDNA Damage
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Mitochondrial damage in aging and apoptosis.

2002

: Mitochondria are essential to cellular aging, and free radical production by mitochondria is increased with aging. The rate of oxidant production by mitochondria correlates inversely with maximal life span of species. In many species, females live longer than males. We report that mitochondrial oxidant production by females is significantly lower than that of males. However, mitochondria from ovariectomized females have a similar oxidant production as those of males. Thus, gender difference in life span can be explained, at least in part, by different oxidant generation by mitochondria. Administration of antioxidants, such as vitamins C and E, or a Ginkgo biloba extract, protects against …

Malemedicine.medical_specialtyMitochondrial DNAAgingApoptosisMitochondrionGeneral Biochemistry Genetics and Molecular Biologychemistry.chemical_compoundHistory and Philosophy of ScienceInternal medicinemedicineAnimalsSex CharacteristicsbiologyLife spanGinkgo bilobaGeneral NeuroscienceGlutathionebiology.organism_classificationMitochondriaRatsOxidative StressEndocrinologyBiochemistrychemistryApoptosisCellular AgingOvariectomized ratFemaleReactive Oxygen SpeciesAnnals of the New York Academy of Sciences
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Mitochondrial oxidant generation is involved in determining why females live longer than males

2006

Females live longer than males in many mammalian species, including humans. This natural phenomenon can be explained on the basis of the mitochondrial theory of aging. Mitochondria are a major source of free radicals in cells. Mitochondria from female rats generate half the amount of hydrogen peroxide than those of males and have higher levels of mitochondrial reduced glutathione. The latter is due to females behaving as double transgenic in over-expressing antioxidant enzymes. Estrogens bind to the estrogen receptors and subsequently activate the mitogen activated protein (MAP) kinase and nuclear factor kappa B (NFkappaB) signalling pathways, resulting in an upregulation of antioxidant enz…

Malemedicine.medical_specialtyMitochondrial DNALongevityEstrogen receptorMitochondrionBiologymedicine.disease_causechemistry.chemical_compoundDownregulation and upregulationInternal medicinemedicineAnimalsHumansSex CharacteristicsEstrogensGlutathioneOxidantsMitochondriaOxidative StressEndocrinologychemistryFemalePhytoestrogensSignal transductionOxidative stressSignal TransductionFrontiers in Bioscience
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Anti-epidermal growth factor receptor therapy in combination with chemoradiotherapy for the treatment of locally advanced anal canal carcinoma: Resul…

2018

Abstract Background and purpose Standard treatment of epidermoid anal cancer is 5-fluorouracil (5FU) and mitomycin C (MMC) based chemoradiotherapy (CRT). This phase I study aims to evaluate the addition of panitumumab (Pmab) to CRT and to determine the maximum tolerated dose (MTD) of Pmab and 5-FU in combination with CRT. Materials and methods Immunocompetent patients with locally advanced tumour without metastases (Stage T2, T3 or T4, whatever N stage; Stage N1–N3 whatever T stage) followed two RT periods (45 Gy in 5 weeks and 20 Gy in 2 weeks, separated by a 2-week break) with concomitant CT sessions of 5FU/MMC at RT weeks 1, 5 and 8. Pmab was administered on RT weeks 1, 3, 5, 8 and 10 ac…

Malemedicine.medical_specialtyMitomycinUrologyPhases of clinical research030218 nuclear medicine & medical imaging03 medical and health sciences0302 clinical medicineAntineoplastic Combined Chemotherapy ProtocolsmedicineHumansAnal cancerPanitumumabRadiology Nuclear Medicine and imagingProspective StudiesAgedbusiness.industryPanitumumabStandard treatmentMitomycin CChemoradiotherapyHematologyMiddle AgedAnus Neoplasmsmedicine.diseaseErbB ReceptorsOncology030220 oncology & carcinogenesisConcomitantT-stageFemaleFluorouracilbusinessChemoradiotherapymedicine.drugRadiotherapy and Oncology
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Effect of dietary supplementation with a mixture of Vitamins C and E on fertilization of tertiary butyl hydroperoxide-treated oocytes and parthenogen…

2002

The present study aims to analyze the effect of dietary supplementation with a mixture of Vitamins C and E on fertilization and later development of tertiary butyl hydroperoxide (tBH)-treated mouse oocytes and on parthenogenetic activation of freshly ovulated mouse oocytes. We fed hybrid mice a standard diet supplemented or not supplemented with Vitamins C and E from the first day of weaning until the age of 12 weeks. We noted no significant effect of diet on fertilization rate, percentage of total and hatching blastocysts, total number of cells, mitotic index and percentage of apoptotic nuclei at 120 h post-insemination of oocytes incubated for 15 min in the presence of 0, 1, 5 and 10 micr…

Malemedicine.medical_specialtyMitotic indexAntioxidantmedicine.medical_treatmentMaturation-Promoting FactorParthenogenesisAscorbic AcidFertilization in VitroWeaningBiologychemistry.chemical_compoundEmbryonic and Fetal DevelopmentMiceHuman fertilizationFood Animalstert-ButylhydroperoxideOral administrationInternal medicineCulture TechniquesmedicineWeaningAnimalsVitamin ESmall AnimalsProtein kinase AEthanolEquineHatchingMice Inbred C57BLEndocrinologychemistryFertilizationMesothelinDietary SupplementsMice Inbred CBAOocytesAnimal Science and ZoologyFemaleMitogen-Activated Protein KinasesTheriogenology
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Acute myeloid leukemia in Italian patients with multiple sclerosis treated with mitoxantrone

2011

none 25 no Abstract OBJECTIVES: To evaluate the incidence and dose-dependency of mitoxantrone (MTX)-associated acute myelocytic leukemia (AML) in the network of Italian multiple sclerosis (MS) clinics. METHODS: We performed a multicenter retrospective cohort study of patients treated with MTX in MS centers under the Italian national health care system between 1998 and 2008. Demographic, disease, treatment, and follow-up information were collected using hospital records. RESULTS: Data were available for 3,220 patients (63% women) from 40 Italian centers. Follow-up (mean ± SD) was 49 ± 29 months (range 12-140 months). We observed 30 cases of AML (incidence 0.93% [95% confidence interval 0.60%…

Malemedicine.medical_specialtyMyeloidmitoxantrone; acute myelocytic leukemia; multiple sclerosisPopulationmultiple sclerosisStatistics NonparametricmitoxantroneFollow-Up StudieArts and Humanities (miscellaneous)Retrospective StudieInternal medicineMultiple SclerosimedicineHumansmultiple sclerosis leukemia mitoxantroneProspective cohort studyeducationRetrospective StudiesAgedAnalgesicseducation.field_of_studyMitoxantroneCumulative dosebusiness.industryMultiple sclerosisIncidence (epidemiology)leukemiaMyeloid leukemiaRetrospective cohort studymedicine.diseaseConfidence intervalSurgeryLeukemiaLeukemia Myeloid Acutemedicine.anatomical_structureItalyCohortSettore MED/26 - NeurologiaAnalgesicFemaleNeurology (clinical)acute myelocytic leukemiaMitoxantronebusinessFollow-Up Studiesmedicine.drugHuman
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Sildenafil reduces neuroinflammation and restores spatial learning in rats with hepatic encephalopathy: underlying mechanisms

2015

Background: There are no specific treatments for the neurological alterations of cirrhotic patients with minimal hepatic encephalopathy (MHE). Rats with MHE due to portacaval shunt (PCS) show impaired spatial learning. The underlying mechanisms remain unknown. The aims of this work were to assess: (a) whether PCS rats show neuroinflammation in hippocampus, (b) whether treatment with sildenafil reduces neuroinflammation and restores spatial learning in PCS rats, and (c) analyze the underlying mechanisms. Methods: Neuroinflammation was assessed by determining inflammatory markers by Western blot. Phosphorylation of MAP-kinase p38 was assessed by immunohistochemistry. Membrane expression of GA…

Malemedicine.medical_specialtyNeurologySildenafilVasodilator AgentsInterleukin-1betaImmunologyHippocampusInflammationPortacaval shuntHippocampusp38 Mitogen-Activated Protein KinasesSildenafil Citratechemistry.chemical_compoundCellular and Molecular NeuroscienceReceptors GABANeuroinflammationmedicineAnimalsRats WistarMaze LearningHepatic encephalopathyNeuroinflammationHepatic encephalopathyInflammationMicrogliaPortacaval Shunt SurgicalTumor Necrosis Factor-alphabusiness.industryResearchGeneral NeuroscienceMacrophage Activationmedicine.diseasehumanitiesSildenafil treatmentRatscGMPmedicine.anatomical_structureCognitive impairmentReceptors Glutamatechemistrynervous systemNeurologyHepatic EncephalopathyMicrogliamedicine.symptombusinesshuman activitiesNeuroscience
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Cannabinoid type 1 receptor blockade promotes mitochondrial biogenesis through endothelial nitric oxide synthase expression in white adipocytes

2008

OBJECTIVE—Cannabinoid type 1 (CB1) receptor blockade decreases body weight and adiposity in obese subjects; however, the underlying mechanism is not yet fully understood. Nitric oxide (NO) produced by endothelial NO synthase (eNOS) induces mitochondrial biogenesis and function in adipocytes. This study was undertaken to test whether CB1 receptor blockade increases the espression of eNOS and mitochondrial biogenesis in white adipocytes. RESEARCH DESIGN AND METHODS—We examined the effects on eNOS and mitochondrial biogenesis of selective pharmacological blockade of CB1 receptors by SR141716 (rimonabant) in mouse primary white adipocytes. We also examined eNOS expression and mitochondrial biog…

Malemedicine.medical_specialtyNitric Oxide Synthase Type IIIEndocrinology Diabetes and MetabolismAdipocytes WhiteImmunoblottingCitrate (si)-SynthaseWhite adipose tissueAMP-Activated Protein KinasesProtein Serine-Threonine KinasesMitochondrionDNA MitochondrialMicechemistry.chemical_compoundAdenosine TriphosphatePiperidinesReceptor Cannabinoid CB1AMP-activated protein kinaseMultienzyme ComplexesEnosAdipocyteInternal medicineInternal MedicinemedicineAnimalsPhosphorylationRNA Small InterferingReceptorCells CulturedDose-Response Relationship DrugbiologyReverse Transcriptase Polymerase Chain ReactionFlow Cytometrybiology.organism_classificationMitochondriaMice Inbred C57BLNitric oxide synthaseMetabolismEndocrinologychemistryMitochondrial biogenesisbiology.proteinSettore BIO/14 - FarmacologiaPyrazolesRimonabant
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Oxidative Inhibition of the Mitochondrial Aldehyde Dehydrogenase Promotes Nitroglycerin Tolerance in Human Blood Vessels

2007

Objectives We tested the hypothesis of whether an inhibition of the nitroglycerin (GTN) bioactivating enzyme mitochondrial aldehyde dehydrogenase (ALDH-2) contributes to GTN tolerance in human blood vessels. Background The hemodynamic effects of GTN are rapidly blunted by the development of tolerance, a phenomenon associated with increased formation of reactive oxygen species (ROS). Recent studies suggest that ROS-induced inhibition of ALDH-2 accounts for tolerance in animal models. Methods Segments of surgically removed arteria mammaria and vena saphena from patients undergoing coronary bypass surgery were used to examine the vascular responsiveness to GTN and the endothelium-dependent vas…

Malemedicine.medical_specialtyNitric Oxide Synthase Type IIIVasodilator AgentsMyocardial InfarctionAldehyde dehydrogenaseVasodilationPharmacologyDrug Administration ScheduleTissue Culture TechniquesNitroglycerinIn vivoEnosmedicineHumansSaphenous VeinEndothelial dysfunctionMammary ArteriesAgedbiologybusiness.industryAldehyde Dehydrogenase MitochondrialDrug ToleranceAldehyde Dehydrogenasemedicine.diseasebiology.organism_classificationAcetylcholineSurgeryOxidative Stressmedicine.anatomical_structureCirculatory systemcardiovascular systembiology.proteinFemaleAnimal studiesbusinessCardiology and Cardiovascular Medicinecirculatory and respiratory physiologyBlood vesselJournal of the American College of Cardiology
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