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Antioxidant properties of UCP1 are evolutionary conserved in mammals and buffer mitochondrial reactive oxygen species.
Free Radical Biol. Med. 77, 210-216 (2014)
Mitochondrial uncoupling reduces reactive oxygen species (ROS) production and appears to be important for cellular signaling/protection, making it a focus for the treatment of metabolic and age-related diseases. While the physiological role of uncoupling protein 1 (UCP1) of brown adipose tissue is established for thermogenesis, the function of UCP1 for the reduction of ROS in cold exposed mice is currently under debate. Here, we investigated the role of UCP1 for mitochondrial ROS handling in the Lesser hedgehog tenrec (Echinops telfairi), a unique proto-endothermic Malagasy mammal with recently identified brown adipose tissue. We show that the reduction of ROS by UCP1 activity also occurs in BAT mitochondria of the tenrec suggesting that the anti-oxidative role of UCP1 is an ancient mammalian trait. Our analysis elucidates that the quantity of UCP1 displays strong control over mitochondrial hydrogen peroxide release while other factors, such as mild cold, nonshivering thermogenesis, oxidative capacity and mitochondrial respiration, do not correlate. Furthermore, hydrogen peroxide release of re-coupled BAT mitochondria associated with mitochondrial membrane potential. These findings led to a model of UCP1 controlling mitochondrial ROS release and, presumably, being controlled by high membrane potential, as proposed in the canonical model of "mild uncoupling", possibly protecting from oxidative stress and maintaining cellular homeostasis. Our study further promotes an ancestral and conserved role of UCP1 in prevention of oxidative stress, which occurred before UCP1 was physiologically integrated into nonshivering thermogenesis, supporting that the ancient evolutionary history of UCP1 dates back to ectothermic vertebrates.
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Publication type
Article: Journal article
Document type
Scientific Article
Keywords
Afrotheria ; Brown Adipose Tissue ; Echinops Telfairi ; Evolution ; Membrane Potential ; Mild Uncoupling ; Protoendothermic ; Reactive Oxygen Species ; Uncoupling Protein 1
ISSN (print) / ISBN
0891-5849
e-ISSN
1873-4596
Quellenangaben
Volume: 77,
Pages: 210-216
Publisher
Elsevier
Publishing Place
New York, NY
Non-patent literature
Publications
Reviewing status
Peer reviewed
Institute(s)
Institute of Diabetes and Obesity (IDO)