Elevated environmental carbon dioxide (pCO₂) levels have been found to cause organ damage in the early life stages of different commercial fish species, including Atlantic cod (Gadus morhua). To illuminate the underlying mechanisms causing pathologies in the intestines, the kidney, the pancreas and the liver in response to elevated pCO₂, we examined related gene expression patterns in Atlantic cod reared for two months under three different pCO₂ regimes: 380 μatm (control), 1800 μatm (medium) and 4200 μatm (high). We extracted RNA from whole fish sampled during the larval (32 dph) and early juvenile stage (46 dph) for relative expression analysis of 18 different genes related to essential metabolic pathways. At 32 dph, larvae subjected to the medium treatment displayed an up-regulation of genes mainly associated with fatty acid and glycogen synthesis (GYS2, 6PGL, ACoA, CPTA1, FAS and PPAR1b). Larvae exposed to the high pCO₂ treatment upregulated fewer but similar genes (6PGL, ACoA and PPAR1b,). These data suggest stress-induced alterations in the lipid and fatty acid metabolism and a disrupted lipid homeostasis in larvae, providing a mechanistic link to the findings of lipid droplet overload in the liver and organ pathologies. At 46 dph, no significant differences in gene expression were detected, confirming a higher resilience of juveniles in comparison to larvae when exposed to elevated pCO₂ up to 4200 μatm.

已经发现，升高的环境二氧化碳（pCO ₂）水平会在包括大西洋鳕（Gadus morhua）在内的各种商业鱼类的生命早期阶段造成器官损害。为了阐明引起pCO ₂升高的肠道，肾脏，胰腺和肝脏病理的潜在机制，我们研究了在三种不同pCO ₂下饲养两个月的大西洋鳕鱼的相关基因表达模式。方案：380μatm（对照），1800μatm（中）和4200μatm（高）。我们从幼虫（32 dph）和少年早期（46 dph）采样的整条鱼中提取RNA，用于18种与基本代谢途径相关的基因的相对表达分析。在32 dph时，经过中等处理的幼虫显示出主要与脂肪酸和糖原合成相关的基因（GYS2、6PGL，ACoA，CPTA1，FAS和PPAR1b）上调。幼虫暴露于高pCO ₂治疗上调了较少但相似的基因（6PGL，ACoA和PPAR1b）。这些数据表明应激诱导的脂质和脂肪酸代谢变化以及幼虫中脂质稳态的破坏，为发现肝脏和器官病理学中脂质滴超负荷提供了机理上的联系。在46 dph时，未检测到基因表达的显着差异，这证实了当幼虫暴露于高达4200μatm的升高的pCO ₂时，其幼虫具有比幼虫更高的弹性。