Adult Killifish Exposure to Crude Oil Perturbs Embryonic Gene Expression and Larval Morphology in First- and Second-Generation Offspring

Exposures to environmental toxicants can have both immediate and long-term impacts, including those that persist into the next generation. Using Gulf killifish (Fundulus grandis), we tested whether adult progenitor exposure to crude oil caused perturbations to larval morphology and embryonic genome-wide gene expression in their first- and second-generation descendants raised in clean water. We also tracked responses of additional direct oil exposure in F1 and F2 embryos. Exposure to oil in progenitor fish caused an altered larval morphology, especially in F2 descendants. Some perturbations observed in descendent fish were enhanced by additional direct oil exposure in lineages with progenitors that had been exposed to oil. Progenitor exposures altered embryonic gene expression in F1 and F2 descendants, implicating impacts on neurological and cardiovascular systems. Molecular responses to progenitor exposure were distinct between F1 and F2 offspring, suggesting complex interactions between mechanisms that contribute to the transgenerational transfer of information. In contrast, molecular responses to additional direct oil exposure during early life development were highly conserved between generations and between progenitor exposure treatments. We conclude that exposure to crude oil causes developmental perturbations that propagate for at least two generations, and we present additional hypotheses about underlying molecular mechanisms and emergent health consequences.

环境有毒物质暴露可引发即时与长期影响，部分效应甚至可延续至下一代。本研究以海湾底鳉（*Fundulus grandis*）为实验对象，探究成年亲鱼暴露于原油环境，是否会对饲养于清洁水体中的子一代（F1）与子二代（F2）后代的幼虫形态及胚胎全基因组基因表达产生扰动。我们同时追踪了F1与F2胚胎额外接受直接原油暴露后的应答情况。

亲代原油暴露会导致后代幼虫形态发生改变，该现象在F2后代中尤为显著。在亲代已暴露于原油的实验谱系中，子代额外接受直接原油暴露会加剧部分观测到的扰动效应。

亲代暴露会改变F1与F2后代的胚胎基因表达模式，提示其对神经系统与心血管系统存在影响。亲代暴露引发的分子应答在F1与F2子代间存在显著差异，表明介导跨代信息传递的各类机制之间存在复杂交互作用。

与之形成鲜明对比的是，生命早期发育阶段额外接受直接原油暴露所触发的分子应答，在不同世代间以及不同亲代暴露处理组间均呈现高度保守性。

本研究证实，原油暴露可引发至少延续两代的发育扰动，并针对其潜在分子机制与潜在健康后果提出了补充假说。