Storey Kenneth B, Storey Janet M
Institute of Biochemistry, Carleton University, 1125 Colonel By Drive, Ottawa, Ontario, K1S 5B6, Canada.
J Exp Biol. 2007 May;210(Pt 10):1700-14. doi: 10.1242/jeb.02716.
Entry into a hypometabolic state is an important survival strategy for many organisms when challenged by environmental stress, including low oxygen, cold temperatures and lack of food or water. The molecular mechanisms that regulate transitions to and from hypometabolic states, and stabilize long-term viability during dormancy, are proving to be highly conserved across phylogenic lines. A number of these mechanisms were identified and explored using anoxia-tolerant turtles as the model system, particularly from the research contributions made by Dr Peter L. Lutz in his explorations of the mechanisms of neuronal suppression in anoxic brain. Here we review some recent advances in understanding the biochemical mechanisms of metabolic arrest with a focus on ideas such as the strategies used to reorganize metabolic priorities for ATP expenditure, molecular controls that suppress cell functions (e.g. ion pumping, transcription, translation, cell cycle arrest), changes in gene expression that support hypometabolism, and enhancement of defense mechanisms (e.g. antioxidants, chaperone proteins, protease inhibitors) that stabilize macromolecules and promote long-term viability in the hypometabolic state.
当受到包括低氧、低温以及缺乏食物或水等环境压力挑战时，进入低代谢状态是许多生物体重要的生存策略。调节进出低代谢状态的转换以及在休眠期间稳定长期生存能力的分子机制，在系统发育谱系中被证明是高度保守的。利用耐缺氧龟作为模型系统，人们确定并探索了其中一些机制，特别是彼得·L·卢茨博士在其对缺氧大脑中神经元抑制机制的探索中所做出的研究贡献。在此，我们回顾了在理解代谢停滞的生化机制方面的一些最新进展，重点关注诸如为ATP消耗重新组织代谢优先级所采用的策略、抑制细胞功能（如离子泵浦、转录、翻译、细胞周期停滞）的分子控制、支持低代谢的基因表达变化以及增强防御机制（如抗氧化剂、伴侣蛋白、蛋白酶抑制剂）等观点，这些防御机制可稳定大分子并促进在低代谢状态下的长期生存能力。
