Search

Ammonia can easily accumulate in water during the culture period, and the accumulated concentrations can reach high levels, which is one of the main stress factors with severely negative effects on the growth and health of cultured shrimp. Dietary manipulation, such as feeding Ampithoe sp. meal, has been proven to be an effective method for reducing the mortality of Litopenaeus vannamei under sublethal ammonia stress and thus improving the ammonia tolerance of the shrimp, but the underlying mechanism needs to be further studied. In this study, L. vannamei with increased ammonia tolerance (PV_T) were obtained by feeding Ampithoe sp. meal, shrimp not fed Ampithoe sp. meal were used as a control (PV_C), and a comprehensive transcriptome analysis of the response of L. vannamei exposed to ammonia-N at the 50% lethal concentration for 96 h was performed. A total of 318,815,732 clean reads, including 170,156,604 and 148,659,128 clean reads from the shrimp in the PV_T and PV_C groups, were obtained. The expression of genes involved in carbohydrate and lipid metabolism pathways was upregulated in the PV_T group compared with the PV_C group, which indicated that the shrimp in the PV_T group had a higher energy supply level than those in the PV_C group, and this difference was the main cause of the observed improvement in ammonia tolerance. Additionally, the upregulated expression of genes involved in the AMP-activated protein kinase (AMPK) pathway in the PV_T group was responsible for the observed upregulation of the expression of genes involved in the carbohydrate and lipid metabolism pathways. However, among the GO terms that were significantly enriched in the DEGs identified from the comparison of the PV_T and PV_C groups, only one GO term was related to the immune system process. In conclusion, feeding Ampithoe sp. meal to L. vannamei exposed to sublethal ammonia can enhance the carbohydrate and lipid metabolism pathways to increase the energy supply and thus reduce the mortality of the shrimp. [ABSTRACT FROM AUTHOR]

• Ammonia stress can activate the PERK-eIF2α and IRE1-XBP1 pathways in the hepatopancreas of Penaeus vannamei. • Ammonia stress activates the IP 3 R-MCU calcium regulatory pathway in the hepatopancreas of P. vannamei. • There are significant positive correlations among endoplasmic reticulum stress, Ca2+ homeostasis and fatty acid metabolism in the hepatopancreas of P. vannamei exposed to ammonia stress. • The energy supply mode of P. vannamei varies under different concentrations of ammonia. The role of endoplasmic reticulum (ER) stress, Ca2+ homeostasis, and fatty acid metabolism in the environmental adaptation of aquatic animals is significant, but further confirmation of the relationship between these factors is needed. This study aimed to investigate the responses and correlations among ER stress, Ca2+ homeostasis, and fatty acid metabolism in Penaeus vannamei under ammonia stress. A total of 640 P. vannamei weighing 3.0 ± 0.4 g were selected and exposed to different total ammonia concentrations (0 mg/L for the control group and 3.80, 7.60, and 11.40 mg/L for the stress groups). The experiment involved a 96 h ammonia stress period to assess indicators related to ER stress, Ca2+ homeostasis, and fatty acid metabolism. The experimental results revealed that after 12 h, exposure to ammonia induced the ER stress response in the hepatopancreas of the shrimp. The groups exposed to concentrations of 3.8 mg/L and 7.6 mg/L exhibited an increase in ER Ca2+ efflux, a decrease in influx, an elevation in mitochondrial Ca2+ influx, an enhanced energy demand within the organism, and substantial consumption of triglycerides. The 11.3 mg/L group exhibited a significant enhancement in fatty acid metabolism. At 24 h, the ER stress response induced by ammonia in the shrimp exhibited a gradual recovery. In the 7.6 mg/L and 11.3 mg/L groups, the ER Ca2+ influx and efflux exhibited significant enhancements, while the mitochondrial Ca2+ influx decreased and the organism's energy demand increased. Moreover, there was a substantial enhancement in fatty acid metabolism. At 48 h, the ER stress response disappeared in each stress group, ER Ca2+ efflux was reduced, triglycerides were consumed, and the body's energy homeostasis was basically restored. At 96 h, a stress response reoccurred in the ER in each stress group, resulting in increased influx of Ca2+ into the ER, augmented energy demand within the organism, and notable enhancement in fatty acid metabolism. Pearson correlation analysis revealed a significant positive correlation between the NH 3 -N content in the hepatopancreas and the expression of ER stress-related genes, as well as between ER Ca2+ influx/efflux and energy homeostasis/fatty acid metabolism. The findings indicate that the stress induced by ammonia triggers an ER stress response in P. vannamei , resulting in ER Ca2+ efflux and mitochondrial Ca2+ influx, which, in turn, enhances fatty acid metabolism to generate additional energy for adaptation in stressful environments. This study contributes to a deeper understanding of the environmental adaptability of P. vannamei in the context of Ca2+ homeostasis. [ABSTRACT FROM AUTHOR]

Ammonia accumulates in the process of shrimp culture and has a strong toxic effect on shrimp survival, physiological metabolism and immune function. Shrimp can adapt to ammonia stress by regulating lipid metabolism. In the present study, to explore the regulatory mechanism of lipid metabolism in ammonia tolerance of Penaeus vannamei (3.08 ± 0.40 g) based on the energy supply, a 96-h ammonia stress experiment was conducted, and energy homeostasis and lipid metabolism responses in the hepatopancreas, muscle and gills of shrimp were observed at total ammonia concentrations of 0 (control group), 6.42, 32.11, and 64.22 mg/L. The cumulative mortality of shrimp increased significantly with increasing ammonia stress concentration. Exposure to ammonia stress significantly decreased the content of adenosine triphosphate (ATP) and the adenylate energy charge (AEC) in the hepatopancreas, muscle and gills, whereas the relative expression of the AMPK, TOR, and SREBP genes was significantly upregulated. The activities of fatty acid synthase (FAS), acetyl-coenzyme A carboxylase (ACC), and carnitine palmitoyltransferase I (CPT-1) and the peroxisome proliferator-activated receptor-α (PPAR-α) level in the hepatopancreas were significantly increased, whereas the opposite was observed in the muscle and gills. In general, the triglyceride (TG) content of the hepatopancreas increased significantly with increasing ammonia concentration. The results indicated that ammonia stress reduced cellular energy levels in the hepatopancreas, muscle and gills of P. vannamei , thereby inducing the activation of the AMPK signaling pathway in these tissues and resulting in increased levels of lipid decomposition and energy supply in the hepatopancreas. However, the activation of the AMPK pathway did not improve the levels of lipid decomposition or energy supply in the shrimp muscle and gills. • Ammonia stress significantly decreased the ATP content and the AECs in shrimp tissues. • Ammonia stress induced significant upregulation of AMPK, TOR, and SREBP in shrimp tissues. • Fatty acid decomposition and synthesis were enhanced in the hepatopancreas in shrimp exposed to ammonia stress. • The imbalance in energy homeostasis caused by ammonia stress may be an important cause of shrimp death. [ABSTRACT FROM AUTHOR]