Previous study revealed severe toxic effects of ammonia nitrogen on Ruditapes philippinarum including lysosomal instability, disturbed metabolic profiles, gill tissues with damaged structure, and variation of neurotransmitter concentrations. However, the underlying molecular mechanism was not fully understood yet. In the present study, digital gene expression technology (DGE) was applied to globally screen the key genes and pathways involved in the responses to short- and long-term exposures of ammonia nitrogen. Results of DGE analysis indicated that short-term duration of ammonia exposure affected pathways in Dorso-ventral axis formation, Notch signaling, thyroid hormone signaling and protein processing in endoplasmic reticulum. The long-term exposure led to DEGs significantly enriched in gap junction, immunity, signal and hormone transduction, as well as key substance metabolism pathways. Functional research of significantly changed DEGs suggested that the immunity of R. philippinarum was weakened heavily by toxic effects of ammonia nitrogen, as well as neuro-transduction and metabolism of important substances. Taken together, the present study provides a molecular support for the previous results of the detrimental toxicity of ammonia exposure in R. philippinarum, further work will be performed to investigate the specific genes and their certain functions involved in ammonia toxicity to molluscs.

先前的研究表明氨氮对菲律宾蛤仔有严重的毒性作用包括溶酶体不稳定性，新陈代谢紊乱，结构受损的g组织以及神经递质浓度的变化。但是，尚未完全理解潜在的分子机制。在本研究中，数字基因表达技术（DGE）被用于全局筛选与短期和长期暴露于氨氮反应相关的关键基因和途径。DGE分析的结果表明，氨暴露的短期持续时间影响内质网中背腹轴形成，Notch信号传导，甲状腺激素信号传导和蛋白质加工的途径。长期接触导致DEGs在缝隙连接，免疫，信号和激素转导以及关键物质代谢途径中显着丰富。由于氨氮的毒性作用以及重要物质的神经传导和新陈代谢，菲律宾蛤仔被严重削弱。综上所述，本研究为以前对菲律宾蛤中氨暴露的有害毒性的研究结果提供了分子支持，将进行进一步的工作以研究涉及氨对软体动物毒性的特定基因及其某些功能。