Stapp L S, Kreiss C M, Pörtner H O, Lannig G
Integrative Ecophysiology, Alfred Wegener Institute Helmholtz-Centre for Polar- & Marine Research, Am Handelshafen 12, D-27570 Bremerhaven, Germany; University of Bremen, NW 2, Leobener Str., 28359 Bremen, Germany.
Integrative Ecophysiology, Alfred Wegener Institute Helmholtz-Centre for Polar- & Marine Research, Am Handelshafen 12, D-27570 Bremerhaven, Germany; University of Bremen, NW 2, Leobener Str., 28359 Bremen, Germany.
Comp Biochem Physiol A Mol Integr Physiol. 2015 Sep;187:160-7. doi: 10.1016/j.cbpa.2015.05.009. Epub 2015 May 22.
Ocean acidification impacts fish and other marine species through increased seawater PCO2 levels (hypercapnia). Knowledge of the physiological mechanisms mediating effects in various tissues of fish is incomplete. Here we tested the effects of extracellular hypercapnia and acidosis on energy metabolism of gill and liver cells of Atlantic cod. Exposure media mimicked blood conditions in vivo, either during normo- or hypercapnia and at control or acidic extracellular pH (pHe). We determined metabolic rate and energy expenditure for protein biosynthesis, Na(+)/K(+)-ATPase and H(+)-ATPase and considered nutrition status by measurements of metabolic rate and protein biosynthesis in media with and without free amino acids (FAA). Addition of FAA stimulated hepatic but not branchial oxygen consumption. Normo- and hypercapnic acidosis as well as hypercapnia at control pHe depressed metabolic stimulation of hepatocytes. In gill cells, acidosis depressed respiration independent of PCO2 and FAA levels. For both cell types, depressed respiration was not correlated with the same reduction in energy allocated to protein biosynthesis or Na(+)/K(+)-ATPase. Hepatic energy expenditure for protein synthesis and Na(+)/K(+)-ATPase was even elevated at acidic compared to control pHe suggesting increased costs for ion regulation and cellular reorganization. Hypercapnia at control pHe strongly reduced oxygen demand of branchial Na(+)/K(+)-ATPase with a similar trend for H(+)-ATPase. We conclude that extracellular acidosis triggers metabolic depression in gill and metabolically stimulated liver cells. Additionally, hypercapnia itself seems to limit capacities for metabolic usage of amino acids in liver cells while it decreases the use and costs of ion regulatory ATPases in gill cells.
海洋酸化通过海水PCO2水平升高（高碳酸血症）影响鱼类和其他海洋物种。关于介导鱼类各种组织效应的生理机制的了解尚不完整。在这里，我们测试了细胞外高碳酸血症和酸中毒对大西洋鳕鱼鳃和肝细胞能量代谢的影响。暴露介质模拟了体内正常或高碳酸血症期间以及对照或酸性细胞外pH（pHe）下的血液状况。我们测定了蛋白质生物合成、Na(+)/K(+)-ATP酶和H(+)-ATP酶的代谢率和能量消耗，并通过测量有或无游离氨基酸（FAA）的培养基中的代谢率和蛋白质生物合成来考虑营养状况。添加FAA刺激肝脏而非鳃的氧气消耗。正常和高碳酸性酸中毒以及对照pHe下的高碳酸血症抑制了肝细胞的代谢刺激。在鳃细胞中，酸中毒抑制呼吸，与PCO2和FAA水平无关。对于这两种细胞类型，呼吸抑制与分配给蛋白质生物合成或Na(+)/K(+)-ATP酶的能量减少不相关。与对照pHe相比，酸性条件下肝脏用于蛋白质合成和Na(+)/K(+)-ATP酶的能量消耗甚至升高，表明离子调节和细胞重组的成本增加。对照pHe下的高碳酸血症强烈降低了鳃Na(+)/K(+)-ATP酶的氧气需求，H(+)-ATP酶也有类似趋势。我们得出结论，细胞外酸中毒会引发鳃和代谢受刺激的肝细胞中的代谢抑制。此外，高碳酸血症本身似乎限制了肝细胞中氨基酸代谢利用的能力，同时降低了鳃细胞中离子调节ATP酶的使用和成本。
