Project description:Saline is a key environmental parameter in aquaculture. Research on acute salinity stress can help farmers determine the optimal salinity level to reduce stress responses in fish larvae, improve survival rates, and increase production efficiencies. It can also aid in the selection or breeding of species suited to environments with specific salinities. However, the molecular mechanisms underlying the negative effects of high salinity on Pseudobagras ussuriensis and the regulatory mechanisms underlying its tolerance remain unclear. In this study, Pseudobagras ussuriensis was exposed to 10 g/L NaCl for 96 h, and the physiological and biochemical changes in the gill and kidney tissues were continuously monitored. Transcriptomic and metabolomic analyses of the gill and kidney tissues were conducted at 24 h to elucidate the molecular adaptation mechanisms to salt stress. A total of 2,554 differentially expressed genes (DEGs) were identified in gill and 1,066 DEGs in the kidney tissue, respectively. Compared with the control group, 826 genes were upregulated and 1,728 were downregulated in the gill tissue under acute salinity stress at 24 h, whereas 508 genes were upregulated and 558 were downregulated in the kidney tissue. These DEGs were involved in oxidative stress, energy metabolism, ion transport, and immune responses. Metabolomic analysis showed that compared to the control group, 85 differential metabolites (DMs) were identified in the gill tissue, with 49 upregulated and 36 downregulated, whereas 433 DMs were identified in the kidney tissue, with 252 upregulated and 181 downregulated. Notably, the levels of phosphatidylcholine (PC) and phosphatidylethanolamine (PE) in the kidney and phosphatidic acid (PA) and PC in the gills were significantly increased, while sphingomyelin (SM) decreased. Integrated analysis of metabolomics and transcriptomics through the KGML network map revealed the downregulation of ALDH, ALDH7A1, AOX, and HADHA in the gill, and ENPP1_3, CD203, L-glutamine (downregulated), and Succinic Acid (upregulated) in the kidney. This study combined metabolomics, transcriptomics, and physiological-biochemical analyses to provide new insights into the molecular mechanisms of oxidative stress, energy metabolism, and immune regulation in gill and kidney tissues under acute salinity stress.

Project description:High ammonia nitrogen stress markedly decreases the survival rate of Litopenaeus vannamei under low-salinity conditions. Nevertheless, most available studies have primarily focused on the ammonia nitrogen response of small-sized shrimp under single-stressor exposure or normal seawater salinity. The molecular regulatory mechanisms, metabolic reprogramming characteristics, and crosstalk between key signaling pathways in L. vannamei exposed to high ammonia nitrogen stress at low salinity remain unclear. To elucidate the stress response and its underlying molecular mechanisms of L. vannamei following low-salinity acclimation and subsequent high ammonia nitrogen challenge, shrimp with an initial body weight of approximately 15 g were gradually acclimated from 30ppt to 5ppt salinity and cultured for one week. Subsequently, the shrimp were subjected to high ammonia nitrogen stress at a concentration of 42.32 mg/L for 96 h. Dynamic monitoring of physiological responses to high ammonia nitrogen stress was performed, and the antioxidant and detoxification capacities of the hepatopancreas were further assessed. The results revealed that ammonia stress triggered continuous accumulation of blood ammonia, urea nitrogen, and uric acid. The activities of glutamate dehydrogenase (GDH), glutamine synthetase (GS), γ-glutamyl transferase (γ-GT), and catalase (CAT) in the hepatopancreas presented a compensatory exhaustion pattern, with an initial increase followed by a gradual decline. Meanwhile, the sustained increase in superoxide dismutase (SOD) activity and progressive depletion of glutathione (GSH) disrupted the redox homeostasis, which aggravated the imbalance between oxidation and antioxidant defense systems. This eventually caused a continuous elevation in malondialdehyde (MDA) content and resulted in severe oxidative damage. Correspondingly, the progressive increases in hemolymph ammonia nitrogen, urea nitrogen (UN), and uric acid (UA) indicated sustained ammonia stress and detoxification through both ureogenesis and uricogenesis. Furthermore, three key time points (12 h, 48 h, and 96 h) after acute ammonia nitrogen exposure were selected for subsequent transcriptomic and metabolomic analyses. Based on the reference genome, transcriptomic analysis annotated a total of 25,305 genes, among which 1,239 were novel genes. Metabolomic profiling detected remarkable alterations in lipid metabolites and amino acid derivatives, represented by 2'-Deoxyguanosine, Guanosine, and L-pyroglutamic acid. Integrated transcriptome and metabolome analysis screened out three core functional pathways, namely secretion pathway, basal metabolism pathway, and immune-related pathway. Furthermore, 11 pivotal genes including solute carrier family 4, member 2 (SLC4A3), nicotinamide/nicotinate riboside kinase (NMRK1), gamma-glutamyltranspeptidase (Ggt1), chitinase (CHIA) and mitogen-activated protein kinase (bsk), together with 17 significantly correlated differential metabolites, were finally identified. Considering the actual frequently occurring concentration of acute high ammonia nitrogen stress in intensive estuarine aquaculture, the present study focused on large-sized L. vannamei. Such large-specimen shrimp are not only more sensitive to ammonia nitrogen stress but also have higher economic value. The findings of this study provide practical and targeted theoretical guidance for health regulation and ammonia nitrogen stress mitigation during the middle and late culture stages of high-density farming in estuarine regions.

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