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禁食和再喂养期间骨骼肌线粒体中 HO 生成的阈效应。

Threshold effect in the HO production of skeletal muscle mitochondria during fasting and refeeding.

机构信息

Laboratoire d'Ecologie des Hydrosystèmes Naturels et Anthropisés, UMR 5023 CNRS, Université de Lyon, ENTPE, 69622 Villeurbanne cedex, France

Laboratoire d'Ecologie des Hydrosystèmes Naturels et Anthropisés, UMR 5023 CNRS, Université de Lyon, ENTPE, 69622 Villeurbanne cedex, France.

出版信息

J Exp Biol. 2019 Feb 27;222(Pt 4):jeb196188. doi: 10.1242/jeb.196188.

Abstract

Under nutritional deprivation, the energetic benefits of reducing mitochondrial metabolism are often associated with enhanced harmful pro-oxidant effects and a subsequent long-term negative impact on cellular integrity. However, the flexibility of mitochondrial functioning under stress has rarely been explored during the transition from basal non-phosphorylating to maximal phosphorylating oxygen consumption. Here, we experimentally tested whether ducklings (), fasted for 6 days and subsequently refed for 3 days, exhibited modifications to their mitochondrial fluxes, i.e. oxygen consumption, ATP synthesis, reactive oxygen species generation (ROS) and associated ratios, such as the electron leak (% ROS/O) and the oxidative cost of ATP production (% ROS/ATP). This was carried out at different steady-state rates of oxidative phosphorylation in both pectoralis (glycolytic) and gastrocnemius (oxidative) muscles. Fasting induced a decrease in the rates of oxidative phosphorylation and maximal ROS release. These changes were completely reversed by 3 days of refeeding. Yet, the fundamental finding of the present study was the existence of a clear threshold in ROS release and associated ratios, which remained low until a low level of mitochondrial activity was reached (30-40% of maximal oxidative phosphorylation activity).

摘要

在营养剥夺的情况下,减少线粒体代谢的能量效益通常与增强有害的促氧化剂效应以及随后对细胞完整性的长期负面影响有关。然而,在线粒体从基础非磷酸化向最大磷酸化耗氧量转变的过程中,很少有研究探讨线粒体功能的灵活性。在这里,我们通过实验测试了禁食 6 天并随后再喂食 3 天的雏鸭()是否表现出其线粒体流量的改变,即耗氧量、ATP 合成、活性氧物质生成(ROS)及其相关比值,如电子泄漏(%ROS/O)和 ATP 生成的氧化成本(%ROS/ATP)。这是在胸肌(糖酵解)和腓肠肌(氧化)肌肉中不同的氧化磷酸化稳态速率下进行的。禁食诱导氧化磷酸化和最大 ROS 释放速率降低。这些变化在 3 天的再喂养后完全逆转。然而,本研究的一个重要发现是 ROS 释放和相关比值存在明显的阈值,只有当线粒体活性达到低水平(最大氧化磷酸化活性的 30-40%)时,这些比值才保持较低水平。

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