Salinity induced stress-response in trout blood

LOKE, Kerri; BERNAL, Diego; Saddleback College; Weber State University: Salinity induced stress-response in trout blood

Rainbow trout, Oncorhynchus mykiss, have the ability to migrate over prolonged periods of time (i.e., weeks to months) between freshwater and marine environments. However, in freshwater trout aquaculture, fishes may be exposed to immersions in saline water (10-15 ppt) for short periods of time (i.e., hours). These immersions assist in the removal of ectoparasites and in the reduction of transport-related mortality, however, little is known about the potential physiological molecular stress-response arising from these salinity treatments. During times of stress, trout erythrocytes are capable of expressing heat shock protein 70 (i.e., Hsp70) that helps in the folding of other proteins and maintaining normal cell function. The objective of this investigation was to determine if short-term (2 hr) exposures to higher than normal salinities (i.e., 5, 10, 15, 25 and 35 ppt) increase levels of Hsp70 in trout blood. In addition, total blood plasma osmolarity and chloride concentrations were measured to quantify ion and water flux during the salinity treatments. Hsp70 levels were not found to be significantly different among the salinity treatments but were significantly higher than those of the controls (0 ppt). Total plasma osmolarity was significantly higher in the 35 ppt treatments when compared to control, 5, 10, 15, and 25 ppt treatments. However, chloride levels for the control, 5, 10, and 15 ppt treatments were similar to each other but lower than the 25 and 35 ppt treatments. Our data show that trout can maintain pre-treatment total plasma osmolarity and chloride when exposed to short-term, salinity treatments below 10ppt, but that even at this treatment there is an increase in the level of Hsp70. This suggest that the triggering of a molecular stress response in trout blood may not be initiated by either a higher total plasma osmolarity or elevated chloride levels, but from a secondary physiological response.

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