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Low in vivo brain glucose consumption and high oxidative stress in accelerated aging
Author(s) -
Borrás Consuelo,
Stvolinsky Sergey,
López-Grueso Raúl,
Fedorova Tatiana,
Gambini Juan,
Boldyrev Alexander,
Viña Jose
Publication year - 2009
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2009.06.019
Subject(s) - senescence , oxidative stress , in vivo , brain aging , accelerated aging , aging brain , ageing , endocrinology , positron emission tomography , medicine , chemistry , biology , neuroscience , cognition , genetics
The 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.