Chronic ammonia nitrogen induces integrated metabolic and immune reprogramming in the hepatopancreas of Macrobrachium rosenbergii
摘要
Total ammonia nitrogen (TAN) is a major cellular stressor in intensive Macrobrachium rosenbergii aquaculture; however, the molecular mechanisms underlying hepatopancreatic responses to chronic ammonia exposure remain insufficiently understood. In this study, juvenile prawns were exposed for seven days to TAN concentrations of 0 mg L⁻¹ (control), 2 mg L⁻¹, and 50 mg L⁻¹ under stable environmental conditions (27–28 °C, pH 7.5–8.0, dissolved oxygen 5–6 mg L⁻¹). No mortality was observed in the control group (100.0 ± 0.0%), while survival in the 2 mg L⁻¹ TAN group was slightly reduced (88.9 ± 3.2%) but not significantly different from the control (p > 0.05). In contrast, survival declined significantly to 75.0 ± 4.5% in the 50 mg L⁻¹ TAN group (p < 0.05). Moderate TAN exposure (2 mg L⁻¹) significantly altered hepatopancreatic gene expression, with 101 differentially expressed genes (47 up-regulated and 54 down-regulated) identified, primarily associated with extracellular matrix–receptor interactions, focal adhesion, lysosomal function, and phagosome-related processes, indicating epithelial remodeling and enhanced vesicular trafficking. High TAN exposure (50 mg L⁻¹) induced pronounced histopathological damage, including tubular disorganization, melanisation, and hemocyte infiltration, and was associated with 58 differentially expressed genes (26 up-regulated and 32 down-regulated) enriched in lysosomal activity, NOD-like receptor signalling, nitrogen metabolism, apoptosis, and antigen presentation pathways. Consistent with transcriptomic alterations, antioxidant enzyme activities (catalase, superoxide dismutase, and glutathione peroxidase) increased alongside elevated malondialdehyde levels, confirming oxidative stress. Collectively, these findings indicate that M. rosenbergii maintains a lysosome-associated adaptive response under moderate ammonia exposure, whereas higher TAN levels induce oxidative and inflammatory injury, defining critical thresholds of hepatopancreatic resilience.
Graphical abstract