Identification of Single-Nucleotide Polymorphism Markers Associated with Cortisol Response to Crowding in Rainbow Trout
While detectable levels of non-steroidal anti-inflammatory drugs (NSAIDs) have been reported in various aquatic habitats, little is known about the mechanism of action of these pharmaceutical drugs on organisms. Recently we demonstrated that NSAIDs disrupt corticosteroidogenesis in rainbow trout (Oncorhynchus mykiss). As cortisol is a seawater adapting hormone, we hypothesized that exposure to NSAIDs will impair the hyposmoregulatory capacity of this species in seawater. Trout were exposed to either waterborne salicylate or ibuprofen in fresh water for four days and the salinity switched to 50% seawater for two days, followed by 100% seawater and sampled two days later. NSAIDs disturbed the seawater-induced elevation in plasma osmolality and concentrations of Cl(-) and K(+), but not Na(+) in rainbow trout. This was accompanied by enhanced gill glycolytic capacity and reduced liver glycogen content in seawater with NSAIDs, suggesting enhanced metabolic demand to fuel ion pumps. While salicylate did not affect gill Na(+)/K(+)-ATPase activity, ibuprofen inhibited the seawater-induced elevation in gill Na(+)/K(+)-ATPase activity. The drugs also further enhanced the seawater-induced elevation in plasma cortisol concentration; this response was greater with salicylate compared to ibuprofen. There were no changes in the transcript levels of key proteins involved in steroidogenesis with NSAIDs, whereas gill and brain GR protein expression expression was reduced with salicylate. Altogether, salicylate and ibuprofen exposures impaired the hyposmoregulatory capacity of rainbow trout in seawater, but the mode of action of the two drugs in bringing about these changes appears distinct in trout.