Aquatic environmental pollutants have various impacts on aquaculture. Specifically, sulfide has been established as being toxic to aquatic animals including the oriental river prawn Macrobrachium nipponense. In response, the hepatopancreas has been broadly studied, as it plays a pivotal role in arthropod nutrient digestion and absorption, energy supply, and organ development as well as in crustacean immunity. However, the underlying molecular mechanisms of hepatopancreas’s response to sulfide toxicity are still poorly understand. Herein, we used Nova-seq 6000 platform to conduct a comparative transcriptome analysis of gene expression profiles in the hepatopancreas of M. nipponense, while it was under the influence of a semi-lethal sulfide concentration (3.20 mg/L at 48 h). A total of 139 million raw reads were obtained, in which 67,602 transcripts were clustered into 37,041 unigenes for further analysis. After constant sulfide exposure for 48 h, 235 differentially expressed genes, i.e., DEGs (151 up-regulated and 84 down-regulated) were identified in the sulfide treatment group (TGHP) compared with the control group (CGHP). We used GO and KEGG databases to annotate all the DEGs into 1180 functions and 123 pathways, respectively. The metabolic pathways included proximal tubule bicarbonate reclamation, sulfur metabolism, glycolysis and gluconeogenesis, and the TCA cycle; while immune-related pathways contained Ras, Rap1, focal adhesion and platelet activation. Additionally, apoptosis-involved pathways e.g., lysosome, also exhibited remarkable alteration in the presence of sulfide stress. Notably, responses to external stimuli and detoxification genes— such as GSKIP, CRT2, APOD, TRET1, CYP4C3 and HR39— were significantly altered by the sulfide stress, indicating that significant toxicity was transferred through energy metabolism, growth, osmoregulatory processes and immunity. Finally, we demonstrated that in the present of sulfide stress, M. nipponense altered the expression of detoxification- and extracellular stimulation-related genes, and displayed positive resistance via tight junction activation and lysosome pathways. The results of these novel experiments shed light on the hepatopancreas’s molecular response to sulfide stress resistance and the corresponding adaptation mechanism; and enable us to identify several potential biomarkers for further studies.

水生环境污染物对水产养殖有多种影响。具体而言，已确定硫化物对包括东方河虾对虾（Macrobrachium nipponense）在内的水生动物有毒。作为回应，肝胰腺已被广泛研究，因为它在节肢动物营养物质的消化和吸收，能量供应，器官发育以及甲壳类动物免疫中起着关键作用。但是，肝胰腺对硫化物毒性反应的潜在分子机制仍知之甚少。本文中，我们使用Nova-seq 6000平台对日本分枝杆菌的肝胰腺中的基因表达谱进行了转录组分析。，同时受到半致死硫化物浓度（48 h时为3.20 mg / L）的影响。总共获得了1.39亿个原始读物，其中67,602个转录物被聚集成到37,041个单基因中，以进行进一步分析。连续暴露48 h硫化物后，与对照组（CGHP）相比，在硫化物治疗组（TGHP）中鉴定出235个差异表达的基因，即DEG（151个上调和84个下调）。我们使用GO和KEGG数据库将所有DEG分别注释为1,180个功能和123个路径。代谢途径包括近端小管碳酸氢盐回收，硫代谢，糖酵解和糖异生以及TCA循环。而与免疫相关的途径包括Ras，Rap1，黏着斑和血小板活化。此外，涉及凋亡的途径，例如溶酶体，在存在硫化物应力的情况下也表现出显着的变化。值得注意的是，硫化物胁迫显着改变了对外部刺激和解毒基因（如GSKIP，CRT2，APOD，TRET1，CYP4C3和HR39）的反应，表明明显的毒性通过能量代谢，生长，渗透压调节和免疫力转移。最后，我们证明了在存在硫化物应力的情况下，N. nipponense改变了排毒和细胞外刺激相关基因的表达，并通过紧密连接激活和溶酶体途径表现出正抗性。这些新颖实验的结果阐明了肝胰腺对硫化物抗逆性的分子反应以及相应的适应机制。并使我们能够确定几种潜在的生物标记物，以进行进一步的研究。