背景:镉(Cd)随着工业和农业污染流入海洋,并显着影响经济头足类动物的生长和发展,例如Sepiaesculenta,五角鱼,还有LoligoJaponica.截至目前,Cd影响esculenta生长发育的原因尚不清楚。
结果:在这项研究中,利用转录组和四个氧化和毒性指标分析了Cd暴露的S.esculenta幼虫的毒理机制。指示性结果表明,Cd引起氧化应激和金属毒性。功能富集分析结果表明,幼虫离子转运,细胞粘附,一些消化和吸收过程受到抑制,细胞功能受损。采用蛋白质-蛋白质相互作用网络综合分析和京都基因和基因组百科全书(KEGG)富集分析,我们发现在确定的20个关键基因中,14个基因与神经毒性有关。它们中的大多数下调并富集到神经活性配体-受体相互作用信号通路,暗示幼虫的神经系统可能会被破坏,和增长,发展,Cd暴露后,运动过程受到显著影响。
结论:S.镉暴露后,esculenta幼虫遭受严重的氧化损伤,这可能会抑制消化和吸收功能,破坏神经系统的稳定性.我们的结果为了解暴露于重金属的幼虫毒理学机制奠定了基础,促进无脊椎动物环境毒理学的发展,并为S.esculenta人工培养提供理论支持。
BACKGROUND: Cadmium (Cd) flows into the ocean with industrial and agricultural pollution and significantly affects the growth and development of economic cephalopods such as Sepia esculenta, Amphioctopus fangsiao, and Loligo japonica. As of now, the reasons why Cd affects the growth and development of S. esculenta are not yet clear.
RESULTS: In this study, transcriptome and four oxidation and toxicity indicators are used to analyze the toxicological mechanism of Cd-exposed S. esculenta larvae. Indicator results indicate that Cd induces oxidative stress and metal toxicity. Functional enrichment analysis results suggest that larval ion transport, cell adhesion, and some digestion and absorption processes are inhibited, and the cell function is damaged. Comprehensive analysis of protein-protein interaction network and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis was used to explore S. esculenta larval toxicological mechanisms, and we find that among the 20 identified key genes, 14 genes are associated with neurotoxicity. Most of them are down-regulated and enriched to the neuroactive ligand-receptor interaction signaling pathway, suggesting that larval nervous system might be destroyed, and the growth, development, and movement process are significantly affected after Cd exposure.
CONCLUSIONS: S. esculenta larvae suffered severe oxidative damage after Cd exposure, which may inhibit digestion and absorption functions, and disrupt the stability of the nervous system. Our results lay a function for understanding larval toxicological mechanisms exposed to heavy metals, promoting the development of invertebrate environmental toxicology, and providing theoretical support for S. esculenta artificial culture.