Phenanthrene is a low molecular weight polycyclic aromatic hydrocarbon (PAH) that is composed of three fused benzene rings. PAHs are formed naturally through incomplete combustion of organic materials, and are environmental contaminants due to anthropogenic activities (e.g. oil extraction and refining, industrial and municipal effluents, fossil fuel burning). Fish exposed to PAHs such as phenanthrene have been reported to exhibit altered reproductive axis endpoints, however the mechanisms that underlie these responses are not fully characterized. To better understand effects at the mechanistic level, we applied transcriptomics to identify molecular pathways altered after acute exposure to phenanthrene on both a dose and temporal scale. Female fathead minnow (Pimephales promelas) were exposed to an average measured concentration of either 0, 29.8, 389 or 943 μg phenanthrene/L for 24, 48, and 72 h in a static-renewal bioassay. Ovaries were assessed for oocyte distribution as well as in vitro 17β-estradiol production and gene expression for transcripts related to steroidogenesis and estrogen signalling. In addition, the liver transcriptome was measured as this tissue is the primary source of the egg yolk precursor protein vitellogenin. Exposure to 29.8 μg phenanthrene/L increased proportions of the cortical alveolar stage in the ovaries after 48 h while the proportion of cortical alveolar oocyte were decreased in fish exposed to 943 μg phenanthrene/L for 48 h. Phenanthrene did not affect 17β-estradiol production at any time or dose, and did not affect transcripts associated with hormone synthesis nor signalling pathways. In the liver, the transcriptome showed fewer genes in common across time when compared to those transcripts affected by concentration at a single time point. Cholesterol metabolism was the only pathway perturbed in the liver following all comparisons in both the dose and time course experiments. Our data suggest that transcriptome networks associated with hepatic lipid metabolism are rapidly affected by phenanthrene, and this may indirectly reduce resources available for reproductive efforts.

菲是由三个稠合苯环组成的低分子量多环芳烃（PAH）。PAH是通过有机材料的不完全燃烧自然形成的，并且是由于人为活动（例如，石油提取和精炼，工业和市政废水，化石燃料燃烧）引起的环境污染物。据报道，暴露于多环芳烃（如菲）的鱼表现出生殖轴终点的变化，但是，尚未完全阐明构成这些反应基础的机制。为了更好地了解在机理水平上的作用，我们应用了转录组学技术来鉴定在急性暴露于菲时在剂量和时间尺度上均发生改变的分子途径。雌性fat鱼min鱼（Pimephales promelas）在静态更新生物测定中分别暴露于0、29.8、389或943μg菲/ L的平均测量浓度下24、48和72小时。评估卵巢的卵母细胞分布以及体外与类固醇生成和雌激素信号转导相关的转录本的17β-雌二醇生成和基因表达。另外，测量了肝转录组，因为该组织是蛋黄前体蛋白卵黄蛋白原的主要来源。暴露于29.8μg菲/ L可使48 h卵巢中皮质肺泡阶段的比例增加，而暴露于943μg菲/ L 48 h的鱼的皮质肺泡卵母细胞比例降低。菲在任何时间或任何剂量都不会影响17β-雌二醇的产生，也不会影响与激素合成或信号通路相关的转录本。在肝脏中，与受单个时间点浓度影响的那些转录本相比，转录组在整个时间内显示出更少的共同基因。在剂量和时程实验中进行所有比较后，胆固醇代谢是肝脏中唯一扰动的途径。我们的数据表明与菲相关的肝脂质代谢相关的转录组网络会迅速受到影响，这可能间接减少可用于生殖工作的资源。