6533b823fe1ef96bd127e116

RESEARCH PRODUCT

Low in vivo brain glucose consumption and high oxidative stress in accelerated aging

Consuelo BorrasJuan GambiniJose ViñaAlexander A. BoldyrevTatiana N. FedorovaSergey StvolinskyRaúl López-grueso

subject

Positron emission tomographyAgingmedicine.medical_specialtyFree RadicalsCentral nervous systemBiophysicsMice Inbred StrainsStem cellsCarbohydrate metabolismmedicine.disease_causeBiochemistryMiceStructural BiologyIn vivoInternal medicineGeneticsmedicineAnimalsMolecular BiologyFree-radical theory of agingchemistry.chemical_classificationReactive oxygen speciesChemistryBrainCell BiologyAccelerated agingOxidative StressGlucosemedicine.anatomical_structureEndocrinologyImmunologyStem cellOxidative stress

description

AbstractThe validity of the free radical theory of aging has been recently questioned. Our aim was to test whether there is oxidative stress in tissues critically involved in accelerated aging (senescence-accelerated mice, SAM) and whether this correlates with lower glucose consumption in vivo and behavioural tests. Positron emission tomography shows that brains of old SAM-prone animals consume less glucose than young ones. Behavioural characteristics, mitochondrial peroxide production, and damage in both the central nervous system and bone marrow stem cells also indicate that SAM-prone animals age faster than SAM-resistant ones. Our results support the role of the free radical theory of aging in critical tissues involved in aging and that this correlates with glucose consumption.

yearjournalcountryeditionlanguage
2009-06-13FEBS Letters
https://doi.org/10.1016/j.febslet.2009.06.019