0000000000591102

AUTHOR

Beatriz Ferrando

0000-0002-4285-0105

showing 8 related works from this author

Exercise and antioxidant supplements in the elderly

2013

Abstract Both exercise and aging increase reactive oxygen species (ROS), which can result in damage to cells. Aging is the result of damage caused by ROS to the mitochondrial genome in post mitotic cells and numerous studies have demonstrated an increase in ROS or their byproducts with exercise. ROS can cause oxidative stress as they overwhelm the antioxidant cellular defenses. Therefore interventions aimed at limiting or inhibiting ROS production, such as supplementation with antioxidant vitamins, should be able to reduce fatigue during muscle contraction and the rate of formation of aging changes with a consequent reduction of the aging rate and disease pathogenesis. However, it has been …

Cell signalingAgingAntioxidantmedicine.medical_treatmentmedia_common.quotation_subjectPopulationPGC-1αSkeletal musclePhysical Therapy Sports Therapy and RehabilitationPharmacologyBiologymedicine.disease_causeNF-κBchemistry.chemical_compoundmedicineOrthopedics and Sports Medicineeducationmedia_commonchemistry.chemical_classificationeducation.field_of_studyReactive oxygen speciesAdaptationsLongevitySkeletal muscleNF-κBmedicine.anatomical_structurechemistryBiochemistryOxidative stressAntioxidant enzymesOxidative stressJournal of Sport and Health Science
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Inhibition of Xanthine Oxidase by Allopurinol Prevents Skeletal Muscle Atrophy: Role of p38 MAPKinase and E3 Ubiquitin Ligases

2012

International audience; Abstract Top Alterations in muscle play an important role in common diseases and conditions. Reactive oxygen species (ROS) are generated during hindlimb unloading due, at least in part, to the activation of xanthine oxidase (XO). The major aim of this study was to determine the mechanism by which XO activation causes unloading-induced muscle atrophy in ratsand its possible prevention by allopurinol, a well-known inhibitor of this enzyme. For this purpose we studied one of the main redox sensitive signalling cascades involved in skeletal muscle atrophy i.e. p38 MAPKinaseand the expression of two well known muscle specific E3 ubiquitin ligases involved in proteolysis, …

MaleAgingAnatomy and Physiology[SDV]Life Sciences [q-bio]lcsh:MedicineMuscle ProteinsGene ExpressionHindlimbSignal transductionmedicine.disease_causep38 Mitogen-Activated Protein KinasesTripartite Motif Proteinschemistry.chemical_compound0302 clinical medicineMolecular cell biologySignaling in Cellular Processeslcsh:ScienceMusculoskeletal System0303 health sciencesMultidisciplinarySignaling cascadesMuscle BiochemistryAnimal ModelsMuscle atrophy3. Good healthMuscular Atrophymedicine.anatomical_structureBiochemistryHindlimb SuspensionMuscleMedicinemedicine.symptomCellular Typesmedicine.drugResearch Articlemedicine.medical_specialtyXanthine OxidaseMAPK signaling cascadesAllopurinolUbiquitin-Protein LigasesAllopurinolBiology03 medical and health sciencesAtrophyModel OrganismsInternal medicinemedicineAnimalsRats WistarXanthine oxidaseMuscle SkeletalBiology030304 developmental biologySoleus muscleMuscle CellsSKP Cullin F-Box Protein LigasesSuperoxide Dismutaselcsh:RSkeletal musclemedicine.diseaseRatsEnzyme ActivationOxidative StressEndocrinologychemistryRatlcsh:QPhysiological Processes030217 neurology & neurosurgeryOxidative stress
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Allopurinol partially prevents disuse muscle atrophy in mice and humans

2018

AbstractDisuse muscle wasting will likely affect everyone in his or her lifetime in response to pathologies such as joint immobilization, inactivity or bed rest. There are no good therapies to treat it. We previously found that allopurinol, a drug widely used to treat gout, protects muscle damage after exhaustive exercise and results in functional gains in old individuals. Thus, we decided to test its effect in the prevention of soleus muscle atrophy after two weeks of hindlimb unloading in mice, and lower leg immobilization following ankle sprain in humans (EudraCT: 2011-003541-17). Our results show that allopurinol partially protects against muscle atrophy in both mice and humans. The pro…

0301 basic medicineProteasome Endopeptidase Complexmedicine.medical_specialtyScience[SDV]Life Sciences [q-bio]Allopurinolmedicine.medical_treatmentAllopurinolHindlimbBed restArticleMice03 medical and health sciences0302 clinical medicineAtrophyPhysical Conditioning AnimalInternal medicineAnimalsHumansMedicineAnkle InjuriesMuscle SkeletalWastingSoleus muscleMultidisciplinaryUbiquitinbusiness.industryQRmedicine.diseaseMuscular Disorders AtrophicMuscle atrophy3. Good healthGoutMuscular Atrophy030104 developmental biologyEndocrinologyHindlimb SuspensionMedicinemedicine.symptombusiness030217 neurology & neurosurgerymedicine.drugScientific Reports
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Alopurinol y su papel en el tratamiento de la sarcopenia

2014

Resumen La xantina oxidasa (XO) es la enzima que cataliza la oxidacion de hipoxantina a xantina y de esta a acido urico, por lo que desempena un importante papel en el catabolismo de las purinas. El alopurinol, un analogo de las purinas, es un conocido inhibidor de la XO ampliamente utilizado en la practica clinica para el tratamiento de la gota. Estudios recientes indican que el alopurinol reduce el estres oxidativo y mejora la funcion vascular en diversas enfemedades cardiometabolicas, aumenta el tiempo de ejercicio en pacientes con angina de pecho y mejora la eficiencia de la contractilidad miocardica en la insuficiencia cardiaca. La XO tambien ejerce un papel importante en la generacion…

AgingMedicine (miscellaneous)Geriatrics and GerontologyRevista Española de Geriatría y Gerontología
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Rapid hemodilution induced by desmopressin after erythropoietin administration in humans

2011

We have shown that treatment with desmopressin has a very effective hemodilution effect in healthy humans. These results led us to suggest the possible role of desmopressin to mask blood doping in sports. Based on our results, the World Anti-Doping Agency included the desmopressin in the 2011 List of Prohibited Substances and Methods. On this occasion, the aim of our study was to test the desmopressin-induced hemodilution after rHuEpo administration in humans. This was an intra-subject, crossover study in which five physically active males acted as their own controls. A basal blood sample was taken on their first visit to the laboratory. The next day, the subjects began the treatment. They …

medicine.medical_specialtyReticulocytesPLASMA VOLUME EXPANDERS[SDV]Life Sciences [q-bio]Physical Therapy Sports Therapy and RehabilitationHematocrit01 natural sciences03 medical and health sciences0302 clinical medicineBlood dopingInternal medicinemedicineEducación Física y DeportivaHaematocritHemoglobinSTIMULATION INDEXlcsh:Sports medicineDesmopressinHEMOGLOBINmedicine.diagnostic_testbusiness.industry010401 analytical chemistryPlasma volume expanders030229 sport sciencesCrossover study3. Good health0104 chemical sciencesStimulation index and plasma volume expandersEndocrinologyBasal (medicine)HematocritErythropoietinAnesthesiaHemoglobinHEMATOCRITHaemoglobinbusinesslcsh:RC1200-1245hormones hormone substitutes and hormone antagonistsmedicine.drugJournal of Human Sport and Exercise
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Oxidative Stress and Ubiquitin Ligases: their involvement in skeletal muscle atrophy

2015

Introduction Muscle atrophy plays a relevant role in the many very prevalent diseases. Generation of reactive oxygen species (mainly by the xanthine oxidase) and inflammation are two of the main triggers of muscle atrophy. Aim The major aim of our study was to determine the mechanism by which reactive oxygen species activate E3 ubiquitin ligases (MuRF-1 and MAFbx) cause muscle atrophy. Possible prevention by allopurinol, a well-known xanthine oxidase inhibitor widely used in clinical practice; and by indomethacin, a non-steroidal antiinflamatory drug was also studied. Materials and methods Male C57BL/6J mice (3 months old) conditioned by 14 days of hindlimb unloading with or without each tr…

medicine.medical_specialtymedicine.drug_classAllopurinolBiologymedicine.diseaseBiochemistryMuscle atrophyCachexiachemistry.chemical_compoundEndocrinologyAtrophychemistryPhysiology (medical)SarcopeniaInternal medicinemedicinemedia_common.cataloged_instanceEuropean unionmedicine.symptomXanthine oxidaseXanthine oxidase inhibitormedia_commonmedicine.drugFree Radical Biology and Medicine
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Redox regulation of E3 ubiquitin ligases and their role in skeletal muscle atrophy

2015

Muscle atrophy is linked to reactive oxygen species (ROS) production during hindlimb-unloading due, at least in part, to the activation of xanthine oxidase (XO). The major aim of our study was to determine the mechanism by which ROS cause muscle atrophy and its possible prevention by allopurinol, a well-known inhibitor of XO widely used in clinical practice, and indomethacin, a nonsteroidal anti-inflammatory drug. We studied the activation of p38 MAP Kinase and NF-?B pathways, and the expression of two E3 ubiquitin ligases involved in proteolysis, the Muscle atrophy F-Box (MAFb) and Muscle RING Finger-1 (MuRF-1). Male Wistar rats (3 mold) conditioned by 14 days of hindlimb unloading (n=18),…

Soleus musclemedicine.medical_specialtySkeletal muscleAllopurinolHindlimbBiologymedicine.disease_causemedicine.diseaseBiochemistryMuscle atrophychemistry.chemical_compoundmedicine.anatomical_structureEndocrinologyAtrophychemistryBiochemistryPhysiology (medical)Internal medicinemedicinemedicine.symptomXanthine oxidaseOxidative stressmedicine.drugFree Radical Biology and Medicine
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Redox modulation of mitochondriogenesis in exercise. Does antioxidant supplementation blunt the benefits of exercise training?

2015

Physical exercise increases the cellular production of reactive oxygen species (ROS) in muscle, liver, and other organs. This is unlikely due to increased mitochondrial production but rather to extramitochondrial sources such as NADPH oxidase or xanthine oxidase. We have reported a xanthine oxidase-mediated increase in ROS production in many experimental models from isolated cells to humans. Originally, ROS were considered as detrimental and thus as a likely cause of cell damage associated with exhaustion. In the past decade, evidence showing that ROS act as signals has been gathered and thus the idea that antioxidant supplementation in exercise is always recommendable has proved incorrect.…

medicine.medical_specialtyAntioxidantmedicine.medical_treatmentPhysical exerciseBiochemistryAntioxidantsSuperoxide dismutasechemistry.chemical_compoundPhysiology (medical)Internal medicinemedicineAnimalsHumansMuscle SkeletalXanthine oxidaseExercisechemistry.chemical_classificationReactive oxygen speciesOrganelle BiogenesisNADPH oxidasebiologyMuscle adaptationGlutathione peroxidaseAdaptation PhysiologicalMitochondria MuscleOxidative StressEndocrinologychemistryDietary Supplementsbiology.proteinOxidation-ReductionFree Radical Biology and Medicine
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