Department of Ocean Sciences, Memorial University, St. John's, NL A1C 5S7, Canada
Department of Ocean Sciences, Memorial University, St. John's, NL A1C 5S7, Canada.
J Exp Biol. 2019 Nov 27;222(Pt 22):jeb208074. doi: 10.1242/jeb.208074.
In fishes, the effect of O limitation on cardiac mitochondrial function remains largely unexplored. The sablefish () encounters considerable variations in environmental oxygen availability, and is an interesting model for studying the effects of hypoxia on fish cardiorespiratory function. We investigated how hypoxia acclimation (6 months at 40% then 3 weeks at 20% air saturation) and anoxia-reoxygenation affected sablefish cardiac mitochondrial respiration and reactive oxygen species (ROS) release rates using high-resolution fluorespirometry. Further, we investigated how hypoxia acclimation affected the sensitivity of mitochondrial respiration to nitric oxide (NO), and compared mitochondrial lipid and fatty acid (FA) composition between groups. Hypoxia acclimation did not alter mitochondrial coupled or uncoupled respiration, or respiratory control ratio, ROS release rates, or superoxide dismutase activity. However, it increased citrate synthase activity (by ∼20%), increased the sensitivity of mitochondrial respiration to NO inhibition (i.e., the NO IC was 25% lower), and enhanced the recovery of respiration (by 21%) and reduced ROS release rates (by 25-30%) post-anoxia. In addition, hypoxia acclimation altered mitochondrial FA composition [increasing arachidonic acid (20:4ω6) and eicosapentaenoic acid (20:5ω3) proportions by 11 and 14%, respectively], and SIMPER analysis revealed that the phospholipid:sterol ratio was the largest contributor (24%) to the dissimilarity between treatments. Overall, these results suggest that hypoxia acclimation may protect sablefish cardiac bioenergetic function during or after periods of O limitation, and that this may be related to alterations in mitochondrial sensitivity to NO and to adaptive changes in membrane composition (fluidity).
在鱼类中，氧气限制对心脏线粒体功能的影响在很大程度上仍未得到探索。黑貂石斑鱼（）在环境氧气供应方面存在相当大的变化，是研究缺氧对鱼类心肺功能影响的理想模型。我们使用高分辨率荧光法研究了低氧适应（6 个月在 40%，然后在 20%空气饱和度下 3 周）和缺氧-复氧如何影响黑貂石斑鱼心脏线粒体呼吸和活性氧（ROS）释放率。此外，我们研究了低氧适应如何影响线粒体呼吸对一氧化氮（NO）的敏感性，并比较了各组之间的线粒体脂质和脂肪酸（FA）组成。低氧适应并没有改变线粒体偶联或解偶联呼吸、呼吸控制比、ROS 释放率或超氧化物歧化酶活性。然而，它增加了柠檬酸合酶活性（增加约 20%），增加了线粒体呼吸对 NO 抑制的敏感性（即 NO IC 降低了 25%），并增强了呼吸的恢复（增加了 21%）和减少了 ROS 释放率（减少了 25-30%）。此外，低氧适应改变了线粒体 FA 组成[分别增加了花生四烯酸（20:4ω6）和二十碳五烯酸（20:5ω3）的比例 11%和 14%]，SIMPER 分析表明，磷脂：固醇比是处理间差异的最大贡献者（24%）。总的来说，这些结果表明，低氧适应可能在 O 限制期间或之后保护黑貂石斑鱼心脏生物能功能，这可能与线粒体对 NO 的敏感性的改变和膜组成（流动性）的适应性变化有关。
