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Uncoupling protein 1 decreases superoxide production in brown adipose tissue mitochondria.
J. Biol. Chem. 285, 21961-21968 (2010)
In thermogenic brown adipose tissue, uncoupling protein 1 (UCP1) catalyzes the dissipation of mitochondrial proton motive force as heat. In a cellular environment of high oxidative capacity such as brown adipose tissue (BAT), mitochondrial uncoupling could also reduce deleterious reactive oxygen species, but the specific involvement of UCP1 in this process is disputed. By comparing brown adipose tissue mitochondria of wild type mice and UCP1-ablated litter mates, we show that UCP1 potently reduces mitochondrial superoxide production after cold acclimation and during fatty acid oxidation. We address the sites of superoxide production and suggest diminished probability of "reverse electron transport" facilitated by uncoupled respiration as the underlying mechanism of reactive oxygen species suppression in BAT. Furthermore, ablation of UCP1 represses the cold-stimulated increase of substrate oxidation normally seen in active BAT, resulting in lower superoxide production, presumably avoiding deleterious oxidative damage. We conclude that UCP1 allows high oxidative capacity without promoting oxidative damage by simultaneously lowering superoxide production.
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Publication type
Article: Journal article
Document type
Scientific Article
Language
english
Publication Year
2010
HGF-reported in Year
0
ISSN (print) / ISBN
0021-9258
e-ISSN
1083-351X
Quellenangaben
Volume: 285,
Issue: 29,
Pages: 21961-21968
Publisher
American Society for Biochemistry and Molecular Biology
Reviewing status
Peer reviewed
Institute(s)
Institute of Diabetes and Obesity (IDO)
PubMed ID
20466728
WOS ID
000279702200008
Erfassungsdatum
2010-12-31