Criscuolo François, Gonzalez-Barroso Maria del Mar, Bouillaud Frederic, Ricquier Daniel, Miroux Bruno, Sorci Gabriele
Université Paris 5, Site NeckerEnfants Malades, Centre National Recherche Scientifique-Unité Propre de Recherche 9078, 156 rue de Vaugirard, 75730 Paris Cedex 15, France.
Am Nat. 2005 Dec;166(6):686-99. doi: 10.1086/497439. Epub 2005 Oct 11.
Reactive oxygen species (ROS)-induced damage on host cells and molecules has been considered the most likely proximal mechanism responsible for the age-related decline in organismal performance. Organisms have two possible ways to reduce the negative effect of ROS: disposing of effective antioxidant defenses and minimizing ROS production. The unbalance between the amount of ROS produced and the availability of antioxidant defenses determines the intensity of so-called oxidative stress. Interestingly, most studies that deal with the effect of oxidative stress on organismal performance have focused on the antioxidant defense compartment and, surprisingly, have neglected the mechanisms that control ROS production within mitochondria. Uncoupling proteins (UCPs), mitochondrial transporters of the inner membrane, are involved in the control of redox state of cells and in the production of mitochondrial ROS. Given their function, UCPs might therefore represent a major mechanistic link between metabolic activity and fitness. We suggest that by exploring the role of expression and function of UCPs both in experimental as well as in comparative studies, evolutionary biologists may gain better insight into this link.
活性氧（ROS）对宿主细胞和分子造成的损伤被认为是导致生物体机能随年龄下降的最可能的近端机制。生物体有两种可能的方式来减轻ROS的负面影响：具备有效的抗氧化防御机制以及尽量减少ROS的产生。ROS产生量与抗氧化防御机制可用性之间的失衡决定了所谓氧化应激的强度。有趣的是，大多数研究氧化应激对生物体机能影响的研究都集中在抗氧化防御方面，令人惊讶的是，这些研究忽略了线粒体内控制ROS产生的机制。解偶联蛋白（UCPs）是线粒体内膜的转运蛋白，参与细胞氧化还原状态的控制以及线粒体ROS的产生。鉴于它们的功能，UCPs可能因此代表了代谢活动与健康之间的主要机制联系。我们认为，通过在实验研究和比较研究中探索UCPs表达和功能的作用，进化生物学家可能会更好地理解这种联系。
