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线粒体氧化磷酸化反应可克服爬行动物中糖皮质激素诱导的应激

Mitochondrial oxidative phosphorylation response overrides glucocorticoid-induced stress in a reptile.

机构信息

Laboratoire d'Ecologie des Hydrosystèmes Naturels et Anthropisés (U.M.R. CNRS 5023), Université Claude Bernard Lyon1, Université de Lyon, Bd du 11 novembre 1918, Bât. Darwin C, 69622, Villeurbanne Cedex, France.

Sorbonne Université, CNRS, IRD, INRA, Institut d'écologie Et Des Sciences de L'environnement (IEES), Paris, France.

出版信息

J Comp Physiol B. 2022 Nov;192(6):765-774. doi: 10.1007/s00360-022-01454-5. Epub 2022 Aug 3.

DOI:10.1007/s00360-022-01454-5
PMID:35922677
Abstract

Stress hormones and their impacts on whole organism metabolic rates are usually considered as appropriate proxies for animal energy budget that is the foundation of numerous concepts and models aiming at predicting individual and population responses to environmental stress. However, the dynamics of energy re-allocation under stress make the link between metabolism and corticosterone complex and still unclear. Using ectopic application of corticosterone for 3, 11 and 21 days, we estimated a time effect of stress in a lizard (Zootoca vivipara). We then investigated whole organism metabolism, muscle cellular O consumption and liver mitochondrial oxidative phosphorylation processes (O consumption and ATP production) and ROS production. The data showed that while skeletal muscle is not impacted, stress regulates the liver mitochondrial functionality in a time-dependent manner with opposing pictures between the different time expositions to corticosterone. While 3 days exposition is characterized by lower ATP synthesis rate and high HO release with no change in the rate of oxygen consumption, the 11 days exposition reduced all three fluxes of about 50%. Oxidative phosphorylation capacities in liver mitochondria of lizard treated with corticosterone for 21 days was similar to the hepatic mitochondrial capacities in lizards that received no corticosterone treatment but with 40% decrease in HO production. This new mitochondrial functioning allows a better capacity to respond to the energetic demands imposed by the environment but do not influence whole organism metabolism. In conclusion, global mitochondrial functioning has to be considered to better understand the proximal causes of the energy budget under stressful periods.

摘要

应激激素及其对整体生物代谢率的影响通常被认为是动物能量预算的合适替代指标,而能量预算是许多旨在预测个体和种群对环境压力反应的概念和模型的基础。然而,应激下能量再分配的动态使得代谢和皮质酮之间的联系变得复杂且仍不清楚。我们使用皮质酮的异位应用 3、11 和 21 天来估计蜥蜴(Zootoca vivipara)中的应激时间效应。然后,我们研究了整体生物代谢、肌肉细胞 O 消耗和肝脏线粒体氧化磷酸化过程(O 消耗和 ATP 产生)和 ROS 产生。数据表明,虽然骨骼肌不受影响,但应激以时间依赖的方式调节肝脏线粒体功能,皮质酮不同时间暴露的结果相反。虽然 3 天暴露的特点是 ATP 合成速率较低,HO 释放较高,而 O 消耗速率不变,但 11 天暴露使所有三种通量降低了约 50%。用皮质酮处理 21 天的蜥蜴的肝脏线粒体氧化磷酸化能力与未接受皮质酮处理的蜥蜴的肝脏线粒体能力相似,但 HO 产生减少了 40%。这种新的线粒体功能使蜥蜴能够更好地应对环境施加的能量需求,但不影响整体生物代谢。总之,必须考虑整体线粒体功能,以更好地理解应激期能量预算的近端原因。

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本文引用的文献

1
The Relationship between Hormones, Glucose, and Oxidative Damage Is Condition and Stress Dependent in a Free-Living Passerine Bird.在一种自由生活的雀形目鸟类中,激素、葡萄糖和氧化损伤之间的关系取决于条件和应激。
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Oxidative status and metabolic profile in a long-lived bird preparing for extreme endurance migration.在准备进行超长距离耐力迁徙的长寿鸟类中氧化状态和代谢特征。
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Oxidative stress and mitochondrial responses to stress exposure suggest that king penguins are naturally equipped to resist stress.
氧化应激和对压力暴露的线粒体反应表明,帝企鹅天生就有抵抗压力的能力。
Sci Rep. 2019 Jun 12;9(1):8545. doi: 10.1038/s41598-019-44990-x.
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Mitochondrial dynamics in adaptive and maladaptive cellular stress responses.细胞应激反应中的适应性和失调性线粒体动态变化。
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A high-caloric diet rich in soy oil alleviates oxidative damage of skeletal muscles induced by dexamethasone in chickens.高脂肪、富含大豆油的饮食可缓解地塞米松诱导的鸡骨骼肌氧化损伤。
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Stress and corticosteroids regulate rat hippocampal mitochondrial DNA gene expression via the glucocorticoid receptor.应激和皮质类固醇通过糖皮质激素受体调节大鼠海马线粒体DNA基因表达。
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Variation in the link between oxygen consumption and ATP production, and its relevance for animal performance.氧消耗与ATP生成之间联系的变化及其对动物性能的相关性。
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Transcriptional coregulators: fine-tuning metabolism.转录共调节因子:微调新陈代谢。
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