Acute exposure of juvenile cobia Rachycentron canadum to nitrate induces gill, esophageal and brain damage

Abstract

Cobia Rachycentron canadum is a fast growing fish with world-wide potential for aquaculture, and has been considered for rearing in recirculating aquaculture systems (RAS). Nitrate is considered the least toxic nitrogenous product in the ammonia nitrification process, but as it may accumulate in RAS, toxic levels can be reached. The objective of this study was to evaluate the acute toxicity and the histopathological effects of nitrate on juvenile cobia. Juveniles (6.87±0.36 g; 11.8±0.19 cm) were acutely exposed to six concentrations of nitrate (500–3000 ppm NO3 −-N) plus a control during 96 h. At the end of this period of exposure, juvenile cobia were sampled for histopathological evaluation. The estimated LC50 of nitrate to juvenile cobia was equal to 2407 and 1829 mg/L NO3 −-N at 24 and 96 h, respectively. Cobia exposed to sub-lethal nitrate concentrations showed histopathologic alterations in the gills, esophagus and brain. The gills revealed epithelial hyperplasia with complete lamellar fusion, telangiectasia, and lamellar shorting induced by necrosis, and the esophagus presented hyperplasia of epithelium and mucus cells. In the brain, glial cells proliferation, satellitosis (microglial cells surrounding neurons with swollen and prenecrotic neurons), and Virchow-Robin spaces (enlarged perivascular spaces, EPVS) were observed. The results of the present study indicate that juvenile cobia have a high tolerance to acute exposure of nitrate. However, assorted histopathological responses were observed for cobia at sub-lethal nitrate concentrations. Therefore, further studies are needed to estimate safe chronic nitrate levels for juvenile cobia culture.