Marine Science Institute, The University of Texas at Austin, Port Aransas, TX 78373, USA.
Marine Science Institute, The University of Texas at Austin, Port Aransas, TX 78373, USA.
Comp Biochem Physiol A Mol Integr Physiol. 2023 Aug;282:111443. doi: 10.1016/j.cbpa.2023.111443. Epub 2023 May 16.
Environmental hypoxia (low dissolved oxygen) is a significant threat facing fishes. As fishes require oxygen to efficiently produce ATP, hypoxia can significantly limit aerobic capacity. However, some fishes show respiratory flexibility that rescues aerobic performance, including plasticity in mitochondrial performance. This plasticity may result in increased mitochondrial efficiency (e.g., less proton leak), increased oxygen storage capacity (increased myoglobin), and oxidative capacity (e.g., higher citrate synthase activity) under hypoxia. We acclimated a hypoxia-tolerant fish, red drum (Sciaenops ocellatus), to 8-days of constant hypoxia to induce a hypoxic phenotype. Fish were terminally sampled for cardiac and red muscle tissue to quantify oxidative phosphorylation, proton leak, and maximum respiration in tissue from both hypoxia-acclimated and control fish. Tissue was also collected to assess the plasticity of citrate synthase enzyme activity and mRNA expression for select oxygen storage and antioxidant pathway transcripts. We found that mitochondrial respiration rates were not affected by hypoxia exposure in cardiac tissue, though citrate synthase activity and myoglobin expression were higher following hypoxia acclimation. Interestingly, measures of mitochondrial efficiency in red muscle significantly improved in hypoxia-acclimated individuals. Hypoxia-acclimated fish had significantly higher OXPHOS Control Efficiency, OXPHOS Capacity and Coupling Control Ratios (i.e., LEAK/OXPHOS). There was no significant change to citrate synthase activity or myoglobin expression in red muscle. Overall, these results suggest that red muscle mitochondria of hypoxia-acclimated fish more efficiently utilize oxygen, which may explain previous reports in red drum of improved aerobic swimming performance in the absence of improved maximum metabolic rate following hypoxia acclimation.
环境缺氧（低溶解氧）是鱼类面临的重大威胁。由于鱼类需要氧气来有效地产生 ATP，因此缺氧会极大地限制有氧能力。然而，一些鱼类表现出呼吸灵活性，可以挽救有氧表现，包括线粒体性能的可塑性。这种可塑性可能导致在缺氧下增加线粒体效率（例如，质子泄漏减少）、增加氧气储存能力（增加肌红蛋白）和氧化能力（例如，柠檬酸合酶活性更高）。我们使一种耐缺氧鱼类——红鼓鱼（Sciaenops ocellatus）适应 8 天的持续缺氧，以诱导缺氧表型。对心脏和红肌组织进行终末采样，以量化缺氧适应和对照鱼组织中的氧化磷酸化、质子泄漏和最大呼吸作用。还收集了组织，以评估柠檬酸合酶酶活性和特定氧气储存和抗氧化途径转录物的 mRNA 表达的可塑性。我们发现，心脏组织中的线粒体呼吸速率不受缺氧暴露的影响，尽管柠檬酸合酶活性和肌红蛋白表达在缺氧适应后更高。有趣的是，红肌中线粒体效率的测量在缺氧适应个体中显著提高。缺氧适应的鱼的 OXPHOS 控制效率、OXPHOS 能力和偶联控制比（即 LEAK/OXPHOS）显著提高。红肌中的柠檬酸合酶活性或肌红蛋白表达没有明显变化。总的来说，这些结果表明，缺氧适应的鱼的红肌线粒体更有效地利用氧气，这可能解释了之前关于红鼓鱼在缺氧适应后有氧游泳性能提高而最大代谢率没有提高的报告。
