UCP3过表达对年轻小鼠与老年小鼠骨骼肌线粒体活性氧生成的影响。
The effect of UCP3 overexpression on mitochondrial ROS production in skeletal muscle of young versus aged mice.
作者信息
Nabben Miranda, Hoeks Joris, Briedé Jacob J, Glatz Jan F C, Moonen-Kornips Esther, Hesselink Matthijs K C, Schrauwen Patrick
机构信息
Department of Human Biology, Nutrition and Toxicology Research Institute Maastricht, Maastricht University, PO Box 616, 6200 MD, Maastricht, The Netherlands.
出版信息
FEBS Lett. 2008 Dec 24;582(30):4147-52. doi: 10.1016/j.febslet.2008.11.016. Epub 2008 Nov 27.
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.
解偶联蛋白3（UCP3）被认为可能通过调节活性氧（ROS）的产生来保护线粒体免受衰老和脂质诱导的损伤。在此我们表明，通过电子自旋共振光谱法评估，过表达UCP3的小鼠（UCP3Tg）在添加4-羟基壬烯醛（4-HNE）后，年龄诱导的ROS产生增加受到抑制。与野生型相比，通过呼吸测定法评估，UCP3Tg小鼠在糖酵解底物上的线粒体功能较低，而在脂肪酸上则倾向于较高。UCP3Tg动物的状态4o呼吸较高。总之，UCP3过表达导致状态4o呼吸增加，并且在存在4-HNE的情况下，抑制年龄诱导的ROS产生增加。
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