Impact of ammonia exposure on coagulation in white shrimp, Litopenaeus vannamei

- Coagulation time of white shrimp exposed to ammonia delayed.
- Ammonia influenced the TG and CP genes expressions in hemocyte.
- Ammonia caused the deficiency coagulation system.

Ammonia (un-ionized plus ionized ammonia as nitrogen), the end product of protein catabolism, is produced by decomposing organic matter. In aquaculture, shrimp are commonly exposed to high concentrations of ammonia that induces immunological and histological changes. The purpose of this study was to evaluate the effects on hemolymph coagulation time, transglutaminase (TG) activity as well as TG and clottable protein (CP) genes expressions in Litopenaeus vannamei when exposed to ambient ammonia-nitrogen (N) at 0, 1, 5, and 10 mg/L for 0, 2, and 7 days. The actual concentrations in control and tests solution were 0.001, 1.15, 5.11, and 11.68 mg/L for ammonia-N, and 7×10−5, 0.080, 0.357, and 0.815 mg/L for NH3-N (unionized ammonia). Delayed coagulation time following exposure to 5 and 10 mg/L of ambient ammonia-N for 7 days, and increased transglutaminase (TG) activity following exposure to 5 and 1 mg/L of ambient ammonia-N for 2 and 7 days, respectively, were observed. Downregulated TG expression and upregulated clottable protein (CP) expression in the hemocytes of L. vannamei exposed to 10 and 5 mg/L of ambient ammonia-N for 2 and 7 days, respectively, were shown. These results indicated that ambient ammonia-N (>5 mg/L) and NH3-N (>0.357 mg/L) interrupted coagulation and down-regulated TG gene expression in L. vannamei, which caused ecotoxicity on immune deficiencies and may contribute the increased susceptibility to infection by pathogens.