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High alkaline environment can lead to respiratory alkalosis and ammonia toxification to freshwater fish. However, the Amur ide (Leuciscus waleckii), which inhabits an extremely alkaline lake in China with titratable alkalinity up to 53.57 mM (pH 9.6) has developed special physiological and molecular mechanisms to adapt to such an environment. Nevertheless, how the Amur ide can maintain acid-base balance and perform ammonia detoxification effectively remains unclear. Therefore, this study was designed to study the ammonia excretion rate (T amm), total nitrogen accumulation in blood and tissues, including identification, expression, and localization of ammonia-related transporters in gills of both the alkali and freshwater forms of the Amur ide. The results showed that the freshwater form Amur ide does not have a perfect ammonia excretion mechanism exposed to high-alkaline condition. Nevertheless, the alkali form of Amur ide was able to excrete ammonia better than freshwater from Amur ide, which was facilitated by the ionocytes transporters (Rhbg , Rhcg1 , Na+/H+ exchanger 2 (NHE2), and V-type H+ ATPase (VHA)) in the gills. Converting ammonia into urea served as an ammonia detoxication strategy to reduced endogenous ammonia accumulation under high-alkaline environment. • Amur ide thrives in extreme alkali-saline lake. • A unique physiological and molecular mechanism for ammonia excretion. • Gill Rh proteins and H+ transporters actively facilitate ammonia excretion. • Decrease in endogenous ammonia accumulation and maintain acid-base balance. [ABSTRACT FROM AUTHOR]

In the present study, the combined effects of hypoxia and nutritional status were examined in common carp ( Cyprinus carpio ), a relatively hypoxia tolerant cyprinid. Fish were either fed or fasted and were exposed to hypoxia (1.5–1.8 mg O 2 L − 1 ) at or slightly above their critical oxygen concentration during 1, 3 or 7 days followed by a 7 day recovery period. Ventilation initially increased during hypoxia, but fasted fish had lower ventilation frequencies than fed fish. In fed fish, ventilation returned to control levels during hypoxia, while in fasted fish recovery only occurred after reoxygenation. Due to this, C. carpio managed, at least in part, to maintain aerobic metabolism during hypoxia: muscle and plasma lactate levels remained relatively stable although they tended to be higher in fed fish (despite higher ventilation rates). However, during recovery, compensatory responses differed greatly between both feeding regimes: plasma lactate in fed fish increased with a simultaneous breakdown of liver glycogen indicating increased energy use, while fasted fish seemed to economize energy and recycle decreasing plasma lactate levels into increasing liver glycogen levels. Protein was used under both feeding regimes during hypoxia and subsequent recovery: protein levels reduced mainly in liver for fed fish and in muscle for fasted fish. Overall, nutritional status had a greater impact on energy reserves than the lack of oxygen with a lower hepatosomatic index and lower glycogen stores in fasted fish. Fasted fish transiently increased Na + /K + -ATPase activity under hypoxia, but in general ionoregulatory balance proved to be only slightly disturbed, showing that sufficient energy was left for ion regulation. [ABSTRACT FROM AUTHOR]

Abstract: Due to eutrophication, high environmental ammonia (HEA) has become a frequent problem in aquatic environments, especially in agricultural or densely populated areas. During certain periods, e.g. winter, feed deprivation may occur simultaneously in natural waters. Additionally, under such stressful circumstances, fish may be enforced to swim at a high speed in order to catch prey, avoid predators and so on. Consequently, fish need to cope with all these stressors by altering physiological processes which in turn are controlled by genes expression. Therefore, in the present study, ammonia toxicity was tested in function of nutrient status (fed versus starved) and swimming performance activity (routine versus exhaustive). Goldfish, a relatively tolerant cyprinid, were exposed to HEA (1mg/L; Flemish water quality guideline for surface water) for a period of 3h, 12h, 1 day, 4 days, 10 days, 21 days and 28 days and were either fed (2% body weight) or starved (kept unfed for 7 days prior to sampling). Results showed that the activity of Na+/K+-ATPase in the gills was stimulated by HEA and disturbance in ion balance was obvious with increases in plasma [Na+], [Cl−] and [Ca2+] after prolonged exposure. Additionally, osmoregulation and metabolism controlling hormones like cortisol and thyroid hormones (T3 and T4) were investigated to understand adaptive responses. The expression kinetics of growth, stress and osmo-regulatory representative genes such as Insulin-like growth factor 1 (IGF-I), growth hormone receptor (GHR), thyroid hormone receptor β (THRβ), prolactin receptor (PRLR), cortisol receptor (CR) and Na+/K+-ATPase α3 were examined. Overall effect of HEA was evident since Na+/K+-ATPase activity, plasma cortisol, Na+ and Ca2+ concentration, expression level of CR and Na+/K+-ATPase α3 mRNA in fed and starved fish were increased. On the contrary, transcript level of PRLR was reduced after 4 days of HEA; additionally T3 level and expression of GHR, IGF-I and THRβ genes were decreased following 10–21 days of HEA. Starvation, the additional challenge in the present study, significantly increased plasma cortisol level and CR transcript level under HEA compared to the fed exposed and control fish. Furthermore, a remarkable reduction in T3 and mRNA levels of THRβ, IGF-I and GHR genes was observed under starvation. The toxic effects in both feeding treatments were exacerbated when imposed to exhaustive swimming with more pronounced effects in starved fish. This confirms that starvation makes fish more vulnerable to external ammonia, especially during exercise. [Copyright &y& Elsevier]

Abstract: This study aimed to elucidate the physiological effects of high environmental ammonia (HEA) following periods of feeding (2% body weight) and starvation (unfed for 7 days prior to sampling) in gold fish (Carassius auratus). Both groups of fish were exposed to HEA (1mg/L; Flemish water quality guideline) for 0h (control), 3h, 12h, 1 day, 4 days, 10 days, 21 days and 28 days. Measurements of weight gain (%), oxygen consumption (MO2), ammonia excretion rate, ammonia quotient (AQ), critical swimming speeds (U crit), plasma and muscle ammonia accumulation, plasma lactate, liver and muscle glycogen, lipid and protein content were done at various time intervals during the experimental periods. Overall, ammonia excretion rates, plasma ammonia accumulation and AQ were significantly affected by food regime in ammonia free water. HEA, the additional challenge in the present study, significantly altered all the studied parameters among fed and starved groups in days-dependent manner. Results show that weight gain (%), MO2, U crit, protein content in liver and muscle, and glycogen content in muscle among starved fish under HEA were considerably reduced compared to control and fed fish. Additionally a remarkable increase in plasma ammonia level, muscle ammonia, lactate accumulation and AQ was seen. However in fed fish, MO2, ammonia excretion rate, AQ and lactate level augmented after exposure to HEA. These results indicate that starved fish appeared more sensitive to HEA than fed fish. Furthermore, as expected, the toxic effect of ammonia exposure in both feeding treatments was exacerbated when imposed to exhaustive swimming (swum at 3/4thU crit). Such effects were more pronounced in starved fish. This suggests that starvation can instigate fish more vulnerable to external ammonia during exercise. Therefore, it was evident from our study that feeding ameliorates ammonia handling and reduces its toxicity during both routine and exhaustive swimming. Moreover, recovery was observed for some physiological parameters (e.g. MO2, ammonia excretion, U crit, plasma ammonia) during the last exposure periods (21–28 days) while for others (e.g. growth, tissue glycogen and protein content, muscle ammonia) effects only became apparent at this time. In the future, these results need to be considered in ecological context as fish in ammonia polluted may experience different phenomenon (starvation and exercise) simultaneously. [Copyright &y& Elsevier]

Rising of temperature in conjunction with acidification due to the anthropogenic climates has tremendously affected all aquatic life. Small changes in the surrounding environment could lead to physiological constraint in the individual. Therefore, this study was designed to investigate the effects of warm water temperature (32 °C) and low pH (pH 6) on physiological responses and growth of hybrid grouper (Epinephelus fuscoguttatus ♀ × Epinephelus lanceolatus ♂) juveniles for 25 days. Growth performance was significantly affected under warm water temperature and low-pH conditions. Surprisingly, the positive effect on growth was observed under the interactive effects of warm water and low pH exposure. Hybrid grouper exposed to the interactive stressor of warm temperature and low pH exhibited higher living cost, where HSI content was greatly depleted to about 2.3-folds than in normal circumstances. Overall, challenge to warm temperature and low pH induced protein mobilization as an energy source followed by glycogen and lipid to support basal metabolic needs. Image 1 •. Effects of warm temperature and/or low water pH were studied. •. Growth performance were negatively impacted to either warm temperature or low pH exposure. •. Interactive exposure of warm temperature and low water pH induced high living cost of hybrid grouper. •. Hybrid grouper adjusted energy metabolism needs to cope with the changing environment. Hybrid grouper modified their physiological responses different to changing environment to compensate growth and metabolic needs. [ABSTRACT FROM AUTHOR]