Chromium is toxic to marine animals and can cause damage to many of their organs, including the liver. To test the toxicity of chromium on marine organisms, we exposed the liver of the marine medaka (Oryzias melastigma) with hexavalent chromium [Cr(VI)]. Our results show that Cr enrichment in the liver demonstrates a positive correlation to the exposure concentration. With the increase of Cr(VI) concentration, pathological changes including nuclear migration, cell vacuolization, blurred intercellular gap, nuclear condensation, become noticeable. To further study changes in gene expression in the liver after Cr(VI) exposure, we used RNA-seq to compare expression profiles before and after Cr(VI) exposure. After acute Cr(VI) exposure (2.61 mg/l) for 96 h, 5862 transcripts significantly changed. It is the first time that the PPAR pathway was found to respond sensitively to Cr(VI) exposure in fish. Finally, combined with other published study, we found that there may be some difference between Cr(VI) toxicity in seawater fish and freshwater fish, due to degree of oxidative stress, distribution patterns and detailed Cr(VI) toxicological mechanisms. Not only does our study explore the mechanisms of Cr(VI) toxicity on the livers of marine medaka, it also points out different Cr(VI) toxicity levels and potential mechanisms between seawater fish and freshwater fish.

铬对海洋动物有毒，可损害包括肝脏在内的许多器官。为了测试铬对海洋生物的毒性，我们暴露了海洋的肝脏（Oryzias melastigma）和六价铬[Cr（VI）]。我们的结果表明，肝脏中铬的富集与暴露浓度呈正相关。随着Cr（VI）浓度的增加，包括核迁移，细胞空泡化，细胞间间隙模糊，核浓缩在内的病理变化变得明显。为了进一步研究Cr（VI）暴露后肝脏中基因表达的变化，我们使用RNA-seq比较了Cr（VI）暴露前后的表达谱。急性Cr（VI）暴露（2.61 mg / l）96小时后，5862个转录本发生了显着变化。这是首次发现PPAR途径对鱼类中的Cr（VI）敏感。最后，结合其他已发表的研究，我们发现海水鱼和淡水鱼中的Cr（VI）毒性之间可能存在一些差异，由于氧化应激的程度，分布模式和详细的Cr（VI）毒理学机理。我们的研究不仅探讨了六价铬对海洋的肝脏的毒性机理，还指出了六价铬的不同毒性水平以及海水鱼和淡水鱼之间的潜在机理。