Due to the heavy fuel oil (HFO) ban in Arctic maritime transport and new legislations restricting the sulphur content of fuel oils, new fuel oil types are continuously developed. However, the potential impacts of these new fuel oil types on marine ecosystems during accidental spills are largely unknown. In this study, we studied the toxicity of three marine fuel oils (two marine gas oils with low sulphur contents and a heavy fuel oil) in early life stages of cod (Gadus morhua). Embryos were exposed for 4 days to water-soluble fractions of fuel oils at concentrations ranging from 4.1 - 128.3 µg TPAH/L, followed by recovery in clean seawater until 17 days post fertilization. Exposure to all three fuel oils resulted in developmental toxicity, including severe morphological changes, deformations and cardiotoxicity. To assess underlying molecular mechanisms, we studied fuel oil-mediated activation of aryl hydrocarbon receptor (Ahr) gene battery and genes related to cardiovascular, angiogenesis and osteogenesis pathways. Overall, our results suggest comparable mechanisms of toxicity for the three fuel oils. All fuel oils caused concentration-dependant increases of cyp1a mRNA which paralleled ahrr, but not ahr1b transcript expression. On the angiogenesis and osteogenesis pathways, fuel oils produced concentration-specific transcriptional effects that were either increasing or decreasing, compared to control embryos. Based on the observed toxic responses, toxicity threshold values were estimated for individual endpoints to assess the most sensitive molecular and physiological effects, suggesting that unresolved petrogenic components may be significant contributors to the observed toxicity.

由于北极海上运输重质燃料油 (HFO) 禁令和限制燃料油硫含量的新立法，新的燃料油类型不断开发。然而，这些新燃料油类型在意外泄漏期间对海洋生态系统的潜在影响在很大程度上是未知的。在本研究中，我们研究了三种船用燃料油（两种含硫量低的船用轻油和一种重质燃料油）在鳕鱼（Gadus morhua）。胚胎在浓度为 4.1 - 128.3 µg TPAH/L 的水溶性燃料油部分中暴露 4 天，然后在清洁海水中恢复，直到受精后 17 天。接触所有三种燃料油都会导致发育毒性，包括严重的形态变化、变形和心脏毒性。为了评估潜在的分子机制，我们研究了燃料油介导的芳烃受体 (Ahr) 基因组激活以及与心血管、血管生成和成骨途径相关的基因。总体而言，我们的结果表明三种燃料油的毒性机制具有可比性。所有燃料油都导致cyp1a mRNA 的浓度依赖性增加，这与ahrr平行，但不是ahr1b转录表达。在血管生成和成骨途径上，与对照胚胎相比，燃料油产生的浓度特异性转录效应要么增加要么减少。根据观察到的毒性反应，估计各个终点的毒性阈值，以评估最敏感的分子和生理效应，这表明未解析的石油成分可能是观察到的毒性的重要贡献者。