Biology Department, University of Ottawa, Ottawa, Ontario, Canada.
Biology Department, University of Ottawa, Ottawa, Ontario, Canada.
Comp Biochem Physiol B Biochem Mol Biol. 2019 Nov;237:110326. doi: 10.1016/j.cbpb.2019.110326. Epub 2019 Aug 26.
Hypoxia-tolerant animals use metabolic suppression as an essential strategy to survive low oxygen. Ectotherms can alter membrane lipid composition in response to changes in environmental temperature, but it is currently unknown whether chronic hypoxia can also elicit membrane restructuring. The goal of this study was to investigate a possible physiological link between membrane remodelling and metabolic suppression in goldfish exposed to prolonged hypoxia (4 weeks at 10% air saturation). We have tested the hypothesis that chronic hypoxia would modulate membrane lipid composition in ways that are consistent with known mechanisms of ion pump inhibition. Because homeoviscous membrane restructuring could interfere with the response to hypoxia, measurements were made at 2 temperatures. Results show that hypoxic goldfish suppress metabolic rate by 74% (at 13 °C) and 63% (at 20 °C). This study is the first to reveal that cold-acclimated animals undergo extensive, tissue-specific restructuring of membrane lipids as they reach minimal metabolic rates. However, hypoxia does not affect membrane composition in fish acclimated to 20 °C. The strong membrane response of cold-acclimated fish involves increases in cholesterol abundance (in white muscle and gills) and in fatty acid saturation, mainly caused by a reduction in %22:6 (docosahexaenoic acid in gills and liver). Major ion pumps like Na/K-ATPase are known to be inhibited by cholesterol and activated by 22:6. Because ion pumping by membrane-bound ATPases accounts for a large fraction of basal cellular energy use, we propose that the membrane responses reported here could be a novel mechanism to promote metabolic suppression in cold-acclimated animals.
耐缺氧动物将代谢抑制作为一种重要策略来在低氧环境中生存。变温动物可以根据环境温度的变化改变膜脂组成，但目前尚不清楚慢性缺氧是否也能引起膜重构。本研究的目的是研究金鱼在长期缺氧（10%空气饱和度 4 周）暴露下，膜重塑和代谢抑制之间可能存在的生理联系。我们检验了这样一个假设，即慢性缺氧会以与离子泵抑制的已知机制一致的方式调节膜脂组成。因为同型粘弹性膜重构可能会干扰对缺氧的反应，所以在 2 个温度下进行了测量。结果表明，缺氧金鱼的代谢率降低了 74%（在 13°C）和 63%（在 20°C）。本研究首次揭示了在达到最低代谢率时，冷水适应动物会经历广泛的、组织特异性的膜脂重排。然而，20°C 适应的鱼类的膜组成不受缺氧影响。冷水适应鱼类强烈的膜反应涉及胆固醇丰度的增加（在白肌和鳃中）和脂肪酸饱和度的增加，主要是由于%22:6（鳃和肝脏中的二十二碳六烯酸）的减少。众所周知，Na/K-ATP 等主要离子泵会被胆固醇抑制，被 22:6 激活。由于膜结合 ATP 酶的离子泵作用占基础细胞能量使用的很大一部分，我们提出这里报告的膜反应可能是促进冷水适应动物代谢抑制的一种新机制。
