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Acute total ammonia nitrogen (TAN) exposure may impair shrimp health, while the interpretation of semicarbazide (SEM) in crustaceans remains uncertain. We examined physiological, histological, omics, and SEM responses to a 96 h toxicity assay and a 48 h graded TAN challenge (0–20 mg/L), with end point hepatopancreas metabolomics and transcriptomics in the control and 20 mg/L groups. The 96 h LC50 was 24.43 mg/L TAN. High TAN caused gill and hepatopancreas lesions, increased apoptosis, and altered amino acid, purine, energy, lipid, and immune-related profiles. SEM was detectable in shell and gill, including control shell, but not in muscle or hepatopancreas under the analytical conditions used. Shell SEM was associated with several stress indices, and nor-NOHA treatment and in vitro oxidation provided exploratory evidence consistent with a possible role of arginine-related metabolism. These data are consistent with a transition from adaptation to injury and endogenous SEM formation under acute TAN stress.
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Long et al. (2026) studied this question.
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