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Salinity stress occurs when salt concentration in the environment changes rapidly, for example because of tidal water flow, rainstorms, drought, or evaporation from small bodies of water. However, gradual changes in salt concentration can also cause osmotic stress in aquatic habitats if levels breach thresholds that reduce the fitness of resident organisms. The latter scenario is exemplified by climate change driven salinization of estuaries and by dilution of ocean surface salinity through changes in the water cycle. In this review, we discuss how fish employ the evolutionarily conserved cellular stress response (CSR) to cope with these different forms of salinity stress. Macromolecular damage is identified as the cause of impaired physiological performance during salinity stress and serves as the signal for inducing a CSR. Basic aspects of the CSR have been observed in fish exposed to salinity stress, including repair and protection of cellular macromolecules, reallocation of energy, cell cycle arrest, and in severe cases, programmed cell death. Osmosensing and signal transduction events that regulate these aspects of the CSR provide a link between environmental salinity and adaptive physiological change required for survival. The CSR has evolved to broaden the range of salinities tolerated by certain euryhaline fish species, but is constrained in stenohaline species that are sensitive to changes in environmental salinity. Knowledge of how the CSR diverges between euryhaline and stenohaline fish enables understanding of physiological mechanisms that underlie salt tolerance and facilitates predictions as to the relative vulnerabilities of different fish species to a rapidly changing hydrosphere., (© 2020 Wiley Periodicals, Inc.)

Nephrocalcinosis is a widespread challenge in intensive production of salmon smolt. There is however no consensus on its aetiology, which makes it problematic to implement proper measures to limit its development. We performed a survey of nephrocalcinosis prevalence and environmental factors in 11 different hatcheries in Mid‐Norway as well as a 6‐month monitoring in one of the hatcheries. A multivariate analysis indicated that the most influencing factor for the prevalence of nephrocalcinosis was the supplementation of sea water during smolt production. In the 6‐month monitoring, the hatchery introduced salinity in the production water prior to the change in day length. Mismatch in those environmental signals may increase the risk for developing nephrocalcinosis. Salinity fluctuations prior to smoltification can cause osmotic stress and result in unbalanced levels of ions in fish blood. This was clearly illustrated in our study, as the fish experienced chronic hypercalcaemia and hypermagnesaemia. Both magnesium and calcium are excreted over the kidneys and it is possible that their prolonged, elevated levels in plasma resulted in an oversaturation of the urine when finally excreted. This again could have led to the aggregation of calcium deposits within the kidney. This study indicates a relationship between osmotic stress induced by salinity changes in juvenile Atlantic salmon and the development of nephrocalcinosis. Other factors that may affect the severity of nephrocalcinosis are currently subjects for discussion. [ABSTRACT FROM AUTHOR]

The present study was designed to examine the physiological responses of juvenile managua cichlid, Cichlasoma managuense under short‐term salinity stress, that is transferring C. managuense from freshwater to brackish water of salinity 0 (control group), 3‰, 6‰, 9‰, 12‰ or 15‰ for 48, 96, 144 and 192 hr respectively. The results showed that gill Na+/K+‐ATPase (NKA) activity revealed a decreased (48 hr), increased (96 hr) and then slightly decreased (144 hr, 192 hr) response with increasing salinity and the lowest NKA level was consistently detected at 9‰ salinity treatment; gill Ca2+/Mg2+‐ATPase (CMA) activities in all salinity treatments were significantly higher than that of the control group (p <.05) before 144 hr; the RNA/DNA ratio was significantly reduced when exposed to high salinities (≥9‰), suggesting growth inhibition; serum cortisol level gradually decreased at low salinities (up to 6‰) but dramatically increased at high salinities of 12‰ and 15‰; and both serum glucose/lactic acid levels and heat shock protein 90 (HSP90) level in liver/muscle were decreased at the salinity between 9‰ and 6‰ but increased at the salinity between 12‰ and 15‰, which was a U‐shape response curve. Taken together, our data suggest that C. managuense can adapt well at salinity up to 0‰–9‰ and high salinity may cause detrimental effects. [ABSTRACT FROM AUTHOR]

Smolting in Atlantic salmon Salmo salar is a critical life‐history stage that is preparatory for downstream migration and entry to seawater that is regulated by abiotic variables including photoperiod and temperature. The present study was undertaken to determine the interaction of temperature and salinity on salinity tolerance, gill osmoregulatory proteins and cellular and endocrine stress in S. salar smolts. Fish were exposed to rapid changes in temperature (from 14 to 17, 20 and 24°C) in fresh water (FW) and seawater (SW), with and without prior acclimation and sampled after 2 and 8 days. Fish exposed simultaneously to SW and 24°C experienced 100% mortality, whereas no mortality occurred in any of the other groups. The highest temperature also resulted in poor ion regulation in SW with or without prior SW acclimation, whereas no substantial effect was observed in FW. Gill Na+–K+‐ATPase (NKA) activity increased in SW fish compared to FW fish and decreased with high temperature in both FW and SW. Gill Nkaα1a abundance was high in FW and Nkaα1b and Na+–K+‐2Cl‐ cotransporter high in SW, but all three were lower at the highest temperature. Gill Hsp70 levels were elevated in FW and SW at the highest temperature and increased with increasing temperature 2 days following direct transfer to SW. Plasma cortisol levels were elevated in SW at the highest temperature. Our results indicate that there is an important interaction of salinity and elevated temperature on osmoregulatory performance and the cellular stress response in S. salar, with an apparent threshold for osmoregulatory failure in SW above 20°C. [ABSTRACT FROM AUTHOR]

Abstract: This study seeks to identify the optimal combination of temperature and salinity for the embryo development of the hybrid groupers, Epinephelus fuscoguttatus (♀) × Epinephelus polyphekadion (♂), using the central composite design and response surface methodology. Results have shown that the low hatching rates of fertilized eggs and high deformity rates of larvae were the result of lower or higher temperature/salinity levels. The linear effects of temperature and salinity were significant in both hatching rates and deformity rates (p < .01). Similar results were observed in the quadratic effects of temperature and salinity (p < .01). Effects of temperature were positively related to salinity effects (p < .05). Salinity effects were more remarkable than temperature on hatching rates, but not the same on deformity rates. Model equations were established for temperature and salinity effects on hatching rates and deformity rates. A high coefficient of determination (R2 > .97) was found for the adequacy and predictive capability of model equations, indicating that these models can be applied to prediction. The optimal combination of temperature and salinity was 27.58°C/30.94, which was derived from the statistical optimization approach. In this condition, the hatching rate was the highest at 85.73%, and the deformity rate was the lowest at 5.96%, with a high desirability function of 0.957. The results of this study can be applied to improve hatching and decrease deformity in future cultures of hybrid groupers. [ABSTRACT FROM AUTHOR]

The aims of this study were to assess whether thermal tolerance of brook trout (Salvelinus fontinalis) is affected during seawater (SW) acclimation and to investigate the role of cortisol in osmoregulation and thermal tolerance duringSWacclimation. Freshwater (FW)-acclimated brook trout at 18°C (Tacc) were exposed to SW for 16 days, whilst maintaining a FW control. Fish were examined for critical thermal maximum (CTmax) 0 (before), 2, 5 and 16 days afterSWexposure, and sampled at Tacc and CTmax for analysis of plasmacortisol, glucose and Cl-, gill Na+/K+-ATPase (NKA) activity and heat shock protein 70 (HSP70) abundance, and whitemusclewater content. At 2 days inSW, CTmax was significantly reduced (from 31 to 26°C), and then recovered by 16 days. This transient decrease in thermal tolerance coincided with a transient increase in plasma Cl- and decrease in muscle moisture content. Salinity itself had no effect on gill HSP70 abundance compared with the large and immediate effects of high temperature exposure during CTmax testing. To examine the role of cortisol in osmoregulation, brook troutwere administered a cortisol implant (5 and 25 μgg-1CORT) prior toSWexposure. Both CORT doses significantly increased their capacity tomaintain plasma Cl- during SW acclimation. Treatment with the 25 μg g-1 CORT dose was shown to significantly improve CTmax after 2 days in SW, and CTmax was associated with plasma Cl- and muscle moisture content. These findings indicate that brook trout are sensitive to temperature during SW acclimation and that thermal tolerance is associated with ion and water balance during SW acclimation. [ABSTRACT FROM AUTHOR]

Stress is a major factor that causes diseases andmortality in the aquaculture industry. The goal was to analyze the expression of stress-related biomarkers in response to different stressors in yellow perch, which is an important aquaculture candidate in North America and highly sensitive to handling in captivity. Three fish groups were established, each having four replicates, and subjected to water temperatures of 14, 20, and 26°C and acute handling stress was performed followed by a salt treatment for 144h at a salinity of 5 ppt. Serum and hepatic mRNA levels of heat shock protein (hsp70), insulin-like growth factor 1 (Igf1), glutathione peroxidase (Gpx), superoxide dismutase 1 (Sod1), and glutathione reductase (Gsr) were quantified at seven times interval over 144 h using ELISA and RT-qPCR. Handling stress caused a significant down-regulation in Hsp70, Gpx, Sod1, and Gsr at a water temperature of 20°C compared to 14 and 26°C. Igf1 was significantly upregulated at 20°C and down-regulated at 14 and 26°C. Salt treatment had a transient reverse effect on the targeted biomarkers in all groups at 72 h, then caused an upregulation after 144 h, compared to the control groups. The data showed a negative strong regulatory linear relationship between igf1 with hsp70 and anti-oxidative gene expressions. These findings could provide valuable new insights into the stress responses that affect fish health and could be used to monitor the stress. [ABSTRACT FROM AUTHOR]

Central Composite Design (CCD) and response surface methodology were used in the experiment to examine the combined effect of temperature (16-28°C) and salinity (18-42) on Hsp70 and IgM genes expression levels in turbot ( Scophthalmus maximus) liver and kidney. The results showed that the coefficients of determination ( R =0.965 2 for liver Hsp70, 0.972 9 for kidney Hsp70, 0.921 for liver IgM and 0.962 1 for kidney IgM) and probability values ( P<0.01) were significant for the regression model. The interactive effect between temperature and salinity on liver Hsp70, kidney Hsp70 and liver IgM were not significant ( P>0.05), while the interactive effect between temperature and salinity on kidney IgM was significant ( P<0.01). The model equation could be used in practice for forecasting Hsp70 and IgM genes expression levels in the liver and kidney of juvenile turbot via applying statistical optimization of the response of interest, at which the maximum liver Hsp70, kidney Hsp70, liver IgM and kidney IgM of 1.48, 1.49, 2.48, and 1.38, respectively, were reached. The present model may be valuable in assessing the feasibility of turbot farming at different geographic locations and, furthermore, could be a useful reference for scientists studying the immunity of turbot. [ABSTRACT FROM AUTHOR]