Seawater carbonate chemistry and processes during experiments with marine mussel, Mytilus galloprovincialis, 2005

In the context of future scenarios of progressive accumulation of anthropogenic CO2 in marine surface waters, the present study addresses the effects of long-term hypercapnia on a Mediterranean bivalve, Mytilus galloprovincialis. Sea-water pH was lowered to a value of 7.3 by equilibration with elevated CO2 levels. This is close to the maximum pH drop expected in marine surface waters during atmosextracellular pHric CO2 accumulation. Intra- and extracellular acid-base parameters as well as changes in metabolic rate and growth were studied under both normocapnia and hypercapnia. Long-term hypercapnia caused a permanent reduction in haemolymph pH. To limit the degree of acidosis, mussels increased haemolymph bicarbonate levels, which are derived mainly from the dissolution of shell CaCO3. Intracellular pH in various tissues was at least partly compensated; no deviation from control values occurred during long-term measurements in whole soft-body tissues. The rate of oxygen consumption fell significantly, indicating a lower metabolic rate. In line with previous reports, a close correlation became evident between the reduction in extracellular pH and the reduction in metabolic rate of mussels during hypercapnia. Analysis of frequency histograms of growth rate revealed that hypercapnia caused a slowing of growth, possibly related to the reduction in metabolic rate and the dissolution of shell CaCO3 as a result of extracellular acidosis. In addition, increased nitrogen excretion by hypercapnic mussels indicates the net degradation of protein, thereby contributing to growth reduction. The results obtained in the present study strongly indicate that a reduction in sea-water pH to 7.3 may be fatal for the mussels. They also confirm previous observations that a reduction in sea-water pH below 7.5 is harmful for shelled molluscs.在人为二氧化碳（anthropogenic CO₂）逐步累积于海洋表层水体的未来情景下，本研究探讨了长期高碳酸血症（hypercapnia）对地中海双壳类动物——地中海贻贝（Mytilus galloprovincialis）的影响。研究通过提升二氧化碳分压实现海水平衡，将海水pH降至7.3，该数值接近大气CO₂累积过程中海洋表层水体预计出现的最大pH降幅。本研究在正常碳酸血症（normocapnia）与高碳酸血症条件下，分别检测了细胞内外酸碱参数、代谢速率与生长状况的变化。 长期高碳酸血症会导致血淋巴（haemolymph）pH持续降低。为缓解酸中毒（acidosis）程度，贻贝会提升血淋巴中的碳酸氢盐水平，而这些碳酸氢盐主要来自贝壳碳酸钙（CaCO₃）的溶解。各组织的细胞内pH至少得到了部分代偿；在对完整软组织进行的长期检测中，其pH未出现与对照组的偏离。 耗氧速率显著下降，表明代谢速率降低。与既往研究结果一致，高碳酸血症下贻贝的细胞外pH降低与代谢速率下降之间存在显著相关性。对生长速率的频率直方图分析显示，高碳酸血症会延缓贻贝生长，这可能与代谢速率下降以及细胞外酸中毒引发的贝壳碳酸钙溶解有关。此外，高碳酸胁迫下贻贝的氮排泄量增加，表明蛋白质发生了净降解，进而加剧了生长减缓。 本研究结果强烈表明，海水pH降至7.3可能对贻贝造成致命影响。同时也验证了既往研究结论：海水pH低于7.5会对带壳软体动物产生危害。