Kreiss Cornelia M, Michael Katharina, Bock Christian, Lucassen Magnus, Pörtner Hans-O
Alfred Wegener Institute, Helmholtz Center for Marine and Polar Research, Integrative Ecophysiology, Am Handelshafen 12, D-27570 Bremerhaven, Germany.
Alfred Wegener Institute, Helmholtz Center for Marine and Polar Research, Integrative Ecophysiology, Am Handelshafen 12, D-27570 Bremerhaven, Germany.
Comp Biochem Physiol A Mol Integr Physiol. 2015 Apr;182:102-12. doi: 10.1016/j.cbpa.2014.12.019. Epub 2014 Dec 19.
Effects of severe hypercapnia have been extensively studied in marine fishes, while knowledge on the impacts of moderately elevated CO2 levels and their combination with warming is scarce. Here we investigate ion regulation mechanisms and energy budget in gills from Atlantic cod acclimated long-term to elevated PCO2 levels (2500 μatm) and temperature (18°C). Isolated perfused gill preparations were established to determine gill thermal plasticity during acute exposures (10-22°C) and in vivo costs of Na(+)/K(+)-ATPase activity, protein and RNA synthesis. Maximum enzyme capacities of F1Fo-ATPase, H(+)-ATPase and Na(+)/K(+)-ATPase were measured in vitro in crude gill homogenates. After whole animal acclimation to elevated PCO2 and/or warming, branchial oxygen consumption responded more strongly to acute temperature change. The fractions of gill respiration allocated to protein and RNA synthesis remained unchanged. In gills of fish CO2-exposed at both temperatures, energy turnover associated with Na(+)/K(+)-ATPase activity was reduced by 30% below rates of control fish. This contrasted in vitro capacities of Na(+)/K(+)-ATPase, which remained unchanged under elevated CO2 at 10°C, and earlier studies which had found a strong upregulation under severe hypercapnia. F1Fo-ATPase capacities increased in hypercapnic gills at both temperatures, whereas Na(+)/K(+)ATPase and H(+)-ATPase capacities only increased in response to elevated CO2 and warming indicating the absence of thermal compensation under CO2. We conclude that in vivo ion regulatory energy demand is lowered under moderately elevated CO2 levels despite the stronger thermal response of total gill respiration and the upregulation of F1Fo-ATPase. This effect is maintained at elevated temperature.
严重高碳酸血症对海水鱼类的影响已得到广泛研究，而关于适度升高的二氧化碳水平及其与升温共同作用的影响的相关知识却很匮乏。在此，我们研究了长期适应高二氧化碳水平（2500微大气压）和温度（18°C）的大西洋鳕鱼鳃中的离子调节机制和能量收支情况。建立了离体灌注鳃标本，以确定急性暴露（10 - 22°C）期间鳃的热可塑性以及体内钠钾ATP酶活性、蛋白质和RNA合成的成本。在粗鳃匀浆中体外测量了F1Fo - ATP酶、氢离子ATP酶和钠钾ATP酶的最大酶活性。在整个动物适应高二氧化碳和/或升温后，鳃部的氧气消耗对急性温度变化的反应更为强烈。分配给蛋白质和RNA合成的鳃呼吸部分保持不变。在两个温度下暴露于二氧化碳的鱼类的鳃中，与钠钾ATP酶活性相关的能量周转率比对照鱼的速率降低了30%。这与钠钾ATP酶的体外活性形成对比，在10°C的高二氧化碳条件下其活性保持不变，而早期研究发现在严重高碳酸血症下其活性有强烈上调。在两个温度下，高碳酸血症鳃中的F1Fo - ATP酶活性均增加，而钠钾ATP酶和氢离子ATP酶活性仅在二氧化碳升高和升温时增加，这表明在二氧化碳条件下不存在热补偿。我们得出结论，尽管鳃总呼吸的热反应更强且F1Fo - ATP酶上调，但在适度升高的二氧化碳水平下，体内离子调节的能量需求仍会降低。这种效应在升高的温度下依然存在。
