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首页> 外文期刊>Marine biology >Effects of long-term acclimation to environmental hypercapnia on extracellular acid-base status and metabolic capacity in Mediterranean fish Sparus aurata
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Effects of long-term acclimation to environmental hypercapnia on extracellular acid-base status and metabolic capacity in Mediterranean fish Sparus aurata

机译：长期适应环境高碳酸血症对地中海鱼类Sparus aurata细胞外酸碱状态和代谢能力的影响

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摘要

In the context of future scenarios of anthropogenic CO_2 accumulation in marine surface waters, the present study addresses the effects of long-term hypercapnia on a Mediterranean fish, Sparus aurata. By equilibration with elevated CO_2 levels seawater pH was lowered to a value of 7.3, close to the maximum pH drop expected in marine surface waters from atmospheric CO_2 accumulation. Intra- and extracellular acid-base parameters as well as changes in enzyme profiles were studied in red and white muscles and the heart under both normocapnia and hypercapnia. The activities of pyruvate kinase (PK), lactate dehydrogenase (L-LDH), citrate synthase (CS), malate dehydrogenase and and 3-hydroxyacyl CoA dehydrogenase (HOAD) reflect the pathways and capacity of oxidative processes in metabolism. Long-term hypercapnia caused a transient reduction in blood plasma pH (pH_e) as well as in intracellular pH (pH_i). Compensation of the acidosis occurred through increased plasma and cellular bicarbonate levels. Changes in enzymatic activities, especially the increase in the activity of L-LDH, paralleled by a drop in CS activity in white and red muscles reflect a shift from aerobic to anaerobic pathways of substrate oxidation during long-term acclimation under hypercapnia. The present results suggest that moderate environmental hypercapnia changes the metabolic profile in tissues of S. aurata. Consequences for slow processes like growth and reproduction potential as well as potential harm at population, species and ecosystem levels require further investigation.
机译：在人为的CO_2在海洋表层水中积聚的未来情况下，本研究解决了长期高碳酸血症对地中海鱼类Sparus aurata的影响。通过与升高的CO_2水平进行平衡，海水的pH值降低到7.3，接近大气CO_2积累在海洋地表水中预期的最大pH下降。在正常和高碳酸血症的情况下，在红色和白色肌肉和心脏中研究了细胞内和细胞外酸碱参数以及酶谱的变化。丙酮酸激酶（PK），乳酸脱氢酶（L-LDH），柠檬酸合酶（CS），苹果酸脱氢酶和3-羟酰基辅酶A脱氢酶（HOAD）的活性反映了代谢中氧化过程的途径和能力。长期高碳酸血症导致血浆pH（pH_e）和细胞内pH（pH_i）暂时降低。酸中毒的补偿通过血浆和细胞碳酸氢盐水平的升高而发生。酶活性的变化，特别是L-LDH活性的增加，与白色和红色肌肉中CS活性的下降相平行，反映了在高碳酸血症下长期适应过程中底物氧化的有氧途径从厌氧途径转变为厌氧途径。目前的结果表明中度环境高碳酸血症改变了金黄色葡萄球菌组织中的代谢谱。诸如生长和繁殖潜力以及对种群，物种和生态系统水平的潜在危害等缓慢过程的后果需要进一步调查。

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