Department of Biology, Faculty of Natural Sciences, Norwegian University of Science and Technology, Trondheim, Norway.
Department of Biological and Environmental Sciences, Faculty of Science, University of Gothenburg, Gothenburg, Sweden.
Physiology (Bethesda). 2023 May 1;38(3):141-158. doi: 10.1152/physiol.00027.2022. Epub 2023 Feb 14.
This review is focused on the questions of why fish exhibit heat failure at thermal extremes and which physiological mechanisms determine the acute upper thermal tolerance. We propose that rapid direct thermal impacts on fish act through three fundamental molecular mechanisms reaction rates, protein structure, and membrane fluidity. During acute warming, these molecular effects then lead to loss of equilibrium and death through various cellular, organ, and physiological pathways. These pathways include mitochondrial dysfunction, oxygen limitation, and impacted excitability of excitable cells and eventually lead to neural and/or muscular failure. The pathways may also lead to loss of homeostasis and subsequent heat failure. There is strong evidence in some species for oxygen limitation in these processes and strong evidence against it in other species and contexts. The limiting mechanisms during acute warming therefore appear to differ between species, life stages, and recent thermal history. We conclude that a single mechanism underpinning the acute upper thermal tolerance across species and contexts will not be found. Therefore, we propose future avenues of research that can elucidate major patterns of physiological thermal limitations in fish.
这篇综述集中讨论了鱼类在极端温度下为何会出现热衰竭以及哪些生理机制决定了鱼类对急性高温的耐受上限这两个问题。我们提出，鱼类会受到快速的直接热冲击，而这些冲击会通过三种基本的分子机制起作用，即反应速率、蛋白质结构和膜流动性。在急性升温过程中，这些分子效应会导致失衡，并通过各种细胞、器官和生理途径导致死亡。这些途径包括线粒体功能障碍、氧气限制以及可兴奋细胞的兴奋性受到影响，最终导致神经和/或肌肉衰竭。这些途径还可能导致体内平衡的丧失和随后的热衰竭。在这些过程中，一些物种有强烈的证据表明存在氧气限制，而在其他物种和情况下则有强烈的证据表明不存在氧气限制。因此，在急性升温过程中，限制机制似乎因物种、生命阶段和近期热历史而异。我们的结论是，不会在跨物种和跨环境的情况下找到单一的机制来支撑鱼类对急性高温的耐受上限。因此，我们提出了未来的研究途径，可以阐明鱼类生理热限制的主要模式。
