摘要
Aquaculture in saline-alkaline waters offers a potential solution to freshwater scarcity while sustaining aquatic production, yet the physiological limits and adaptive mechanisms of cultured species remain insufficiently understood. This study examined the responses of Hong Kong catfish ( Clarias fuscus ), a widely farmed species in southern China, under acute saline-alkaline stress. Fish were exposed for 0, 12, 24, 48, 72, and 96 h to either control water (0 ‰ salinity, 0 mmol/L alkalinity, n = 30) or saline-alkaline water (17 ‰ salinity, 50 mmol/L alkalinity, n = 30). Histological analysis revealed dynamic liver damage, initially characterized by mild vacuolar degeneration and inflammatory infiltration, progressing to a peak at 48 h with marked hepatocellular atrophy and cytoplasmic depletion, followed by partial alleviation during prolonged exposure. Antioxidant enzyme (SOD, CAT, GSH-Px) declined initially, reaching a nadir at 12 h before partially recovering, indicating disruption of redox homeostasis. In contrast, MDA, ALP, ACP, ALT, and AST increased and peaked at 12 h, consistent with lipid peroxidation, and hepatocellular injury. Transcriptome profiling revealed that a total of 6949 DEGs were detected in liver tissue, with functional enrichment pointing to energy metabolism, oxidative phosphorylation, immune response, and protein processing pathways. Notably, thermogenesis and oxidative phosphorylation pathways were predominant at 48 h, while endoplasmic reticulum protein processing pathways were up-regulated at 96 h, indicating a temporal shift from energy metabolism to cellular repair and adaptation. Collectively, these findings demonstrate that acute saline-alkaline stress causes liver injury, perturbs oxidative and immune homeostasis, and reprograms gene expression in C. fuscus , offering critical insights into liver-mediated stress adaptation and metabolic regulation and a basis for optimizing management practices in saline-alkaline aquaculture.
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