Cardiac mitochondrial function, nitric oxide sensitivity and lipid composition following hypoxia acclimation in sablefish
Cardiac mitochondrial function, nitric oxide sensitivity and lipid composition following hypoxia acclimation in sablefish
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DOI：
10.1242/jeb.208074
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发表时间：
2019-11-01
影响因子：
2.8
通讯作者：
Gamperl, Anthony K.
中科院分区：
文献类型：
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作者：
Gerber, Lucie;Clow, Kathy A.;Gamperl, Anthony K.
在鱼类中，O-2 限制对心脏线粒体功能的影响在很大程度上仍未被探索。黑貂鱼（Anoplopoma fimbria）在环境氧气供应方面遇到相当大的变化，并且是研究缺氧对鱼类心肺功能影响的有趣模型。我们使用高分辨率荧光呼吸测定法研究了体内缺氧适应（40％空气饱和度下 6 个月，然后 20％ 空气饱和度下 3 周）和体外缺氧复氧如何影响黑貂鱼心脏线粒体呼吸和活性氧（ROS）释放率。此外，我们研究了缺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。缺氧适应不会改变线粒体偶联或非偶联呼吸、或呼吸控制比、ROS 释放速率、P-50 或超氧化物歧化酶活性。然而，它增加了柠檬酸合酶活性（增加了约20％），增加了线粒体呼吸对NO抑制的敏感性（即NO IC50降低了25％），并增强了缺氧后呼吸的恢复（增加了21％）并降低了ROS释放率（减少了25-30％）。此外，缺氧适应改变了线粒体 FA 组成[花生四烯酸 (20:4 omega 6) 和二十碳五烯酸 (20:5 omega 3) 比例分别增加 11% 和 14%]，SIMPER 分析显示磷脂：甾醇比例是治疗之间差异的最大贡献者 (24%)。总体而言，这些结果表明，缺氧驯化可能会在 O-2 限制期间或之后保护黑貂鱼的心脏生物能功能，这可能与线粒体对 NO 敏感性的改变和膜组成（流动性）的适应性变化有关。
In fishes, the effect of O-2 limitation on cardiac mitochondrial function remains largely unexplored. The sablefish (Anoplopoma fimbria) 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 in vivo hypoxia acclimation (6 months at 40% then 3 weeks at 20% air saturation) and in vitro 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, P-50 or superoxide dismutase activity. However, it increased citrate synthase activity (by similar to 20%), increased the sensitivity of mitochondrial respiration to NO inhibition (i.e., the NO IC50 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 (20:4 omega 6) and eicosapentaenoic acid (20:5 omega 3) 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-2 limitation, and that this may be related to alterations in mitochondrial sensitivity to NO and to adaptive changes in membrane composition (fluidity).