Chronic ammonia toxicity disturbed energy homeostasis and damaged the hepatopancreas of swimming crab Portunus trituberculatus

Abstract

Ammonia is toxic to aquatic animals and its chronic effects on the swimming crab Portunus trituberculatus is still not fully understood. Therefore, we conducted this study to detect the responses of energy metabolism of crabs to chronic high environmental ammonia (HEA) exposure by exposing them to HEA (5 and 15 mg·L−1) for 15 d and subsequently recovering in natural seawater for 7 d. Then we analyzed the glucose and lactate content, ATPases activities and the expression of the genes involved in energy homeostasis. Besides, glutamic pyruvic transaminase (GPT), glutamic oxaloacetic transaminase (GOT), alkaline phosphatase (AKP) activity and histological changes were assayed to determine the HEA-induced hepatopancreas damage. Results showed a HEA dose- and exposure time-dependent mortality and hepatopancreas damage. This was accompanied by a loss of energy homeostasis as indicated by the significant increase of AMP/ATP ratio and genes expression involved in AMPK pathway (P < 0.05). While indices such as HMGCR expression, glucose content and ion related ATPases demonstrated the energy dishomeostasis might be related with the inhibitory effect of chronic HEA on energy regulatory capacity especially when HEA approached 15 mg·L−1. In summary, chronic HEA can seriously damage hepatopancreas structure and function of energy metabolism in P. trituberculatus, and this deleterious effect could even not be completely repaired in a short recovery time.