Energy Metabolism Laboratory, Department of Health Sciences and Technology, Institute of Translational Medicine, Swiss Federal Institute of Technology (ETH) Zurich, Schwerzenbach, Switzerland.
EMBO Rep. 2020 May 6;21(5):e50340. doi: 10.15252/embr.202050340. Epub 2020 Apr 23.
Interventions and small molecules, which promote formation of reactive oxygen species (ROS), have repeatedly been shown to increase stress resistance and lifespan of different model organisms. These phenotypes occur only in response to low concentrations of ROS, while higher concentrations exert opposing effects. This non-linear or hormetic dose-response relationship has been termed mitohormesis, since ROS are mainly generated within the mitochondrial compartment. A report by Matsumura et al in this issue of EMBO Reports now demonstrates that an endogenously formed metabolite, namely N-acetyl-L-tyrosine (NAT), is instrumental in promoting cellular and organismal resilience by inducing mitohormetic mechanisms, likely in an evolutionarily conserved manner [1].
干预措施和小分子可以促进活性氧 (ROS) 的形成，已反复证明它们可以提高不同模式生物的应激抗性和寿命。这些表型仅在低浓度 ROS 的情况下发生，而更高浓度则会产生相反的效果。这种非线性或 hormetic 剂量反应关系被称为线粒体适应，因为 ROS 主要在线粒体区室中产生。松村等人在本期《EMBO 报告》中的报告表明，一种内源性代谢产物，即 N-乙酰-L-酪氨酸 (NAT)，通过诱导线粒体适应机制，可能以进化上保守的方式，在促进细胞和机体的弹性方面发挥重要作用[1]。
