Elevated concentrations of carbon dioxide are a common stressor for fish and other aquatic animals. In particular, intensive aquaculture can impose prolonged periods of severe environmental hypercapnia, manifold exceeding CO₂ concentrations of natural habitats. In order to cope with this stressor, gills are essential and constitute the primary organ in the acclimatization process. Yet, despite a general understanding of changes in ion regulation, not much is known with regard to other cellular mechanisms. In this study, we apply RT-qPCR to investigate changes in the expression of several genes associated with metabolism, stress and immunity within gills of juvenile turbot (Psetta maxima) after an eight-week exposure to different concentrations of CO₂ (low = ∼3000 μatm, medium = ∼15,000 μatm and high = ∼25,000 μatm CO₂). Histological examination of the gill tissue only found a significant increase of hypertrophied secondary lamella in the highest tested treatment level. gene expression results, on the other hand, implied both, mutual and dose-dependent transcriptional adjustments. Comparable up-regulation of IL-1ß, LMP7 and Grim19 at medium and high hypercapnia indicated an increase of reactive oxygen species (ROS) within gill cells. Simultaneous increase in Akirin and PRDX transcripts at medium CO₂ indicated enhanced anti-oxidant activity and regulation of transcription, while reduced mRNA concentrations of COX, EF1α and STAT2 at high CO₂ denoted suppressed protein synthesis and reduced metabolic capacity. In addition to upregulated DFAD and ApoE expression, implying compensating repair measures, gills exposed to the highest tested treatment level seemed to operate close to or even beyond their maximum capacity. Thus, fitting the model of capacity limitation, our results provide evidence for accretive intracellular hypoxia and oxidative stress in the gills of turbot, dependent on the level of environmental hypercapnia. Further, genes, such as COX, may be valuable biomarkers when attempting to discriminate between a successful and an overpowered stress response.

二氧化碳浓度升高是鱼类和其他水生动物的常见压力源。特别是，集约化水产养殖可造成严重的环境高碳酸血症的长期发作，多种多样的自然栖息地超过CO ₂浓度。为了应付这种压力，g是必不可少的，并且是适应过程中的主要器官。然而，尽管对离子调节的变化有一般的了解，但是关于其他细胞机制知之甚少。在这项研究中，我们应用RT-qPCR来研究在8周暴露于不同浓度的CO ₂后，幼体turbo（Psetta maxima）的ill内与代谢，应激和免疫相关的几个基因的表达变化（低=〜3000μatm，中=〜15,000μatm，高=〜25,000μatmCO ₂）。the组织的组织学检查仅发现在最高测试治疗水平下肥大的次生薄片显着增加。另一方面，基因表达的结果暗示了相互和剂量依赖性的转录调节。中，高碳酸血症时，IL-1ß，LMP7和Grim19的相对上调表明indicated细胞内的活性氧（ROS）增加。在中等CO ₂浓度下Akirin和PRDX转录物的同时增加表明在高CO ₂浓度下抗氧化活性和转录调控增强，而COX，EF1α和STAT2的mRNA浓度降低表示抑制了蛋白质合成并降低了代谢能力。除了上调DFAD和ApoE的表达（暗示补偿措施）外，暴露于最高测试水平的g似乎在接近或什至超过其最大处理能力。因此，根据容量限制模型，我们的研究结果为大菱t the内细胞内缺氧和氧化应激的增加提供了证据，具体取决于环境高碳酸血症的水平。此外，当试图区分成功和过度的应激反应时，基因（例如COX）可能是有价值的生物标记。