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The effect of UCP3 overexpression on mitochondrial ROS production in skeletal muscle of young versus aged mice
Author(s) -
Nabben Miranda,
Hoeks Joris,
Briedé Jacob J.,
Glatz Jan F.C.,
Moonen-Kornips Esther,
Hesselink Matthijs K.C.,
Schrauwen Patrick
Publication year - 2008
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.2008.11.016
Subject(s) - ucp3 , reactive oxygen species , respiration , uncoupling protein , mitochondrion , mitochondrial ros , respirometry , chemistry , oxidative phosphorylation , bioenergetics , skeletal muscle , medicine , endocrinology , biology , biochemistry , microbiology and biotechnology , anatomy , adipose tissue , brown adipose tissue
Uncoupling protein 3 (UCP3) is suggested to protect mitochondria against aging and lipid‐induced damage, possibly via modulation of reactive oxygen species (ROS) production. Here we show that mice overexpressing UCP3 (UCP3Tg) have a blunted age‐induced increase in ROS production, assessed by electron spin resonance spectroscopy, but only after addition of 4‐hydroxynonenal (4‐HNE). Mitochondrial function, assessed by respirometry, on glycolytic substrate was lower in UCP3Tg mice compared to wild types, whereas this tended to be higher on fatty acids. State 4o respiration was higher in UCP3Tg animals. To conclude, UCP3 overexpression leads to increased state 4o respiration and, in presence of 4‐HNE, blunts the age‐induced increase in ROS production.