Chronic Toxicity Of Ammonia Research Articles

α-lipoic acid ameliorates hepatotoxicity induced by chronic ammonia toxicity in crucian carp (Carassius auratus gibelio) by alleviating oxidative stress, inflammation and inhibiting ERS pathway

High environment ammonia (HEA) poses a deadly threat to aquatic animals and indirectly impacts human healthy life, while nutritional regulation can alleviate chronic ammonia toxicity. α-lipoic acid exhibits antioxidative effects in both aqueous and lipid environments, mitigating cellular and tissue damage caused by oxidative stress by aiding in the neutralization of free radicals (reactive oxygen species). Hence, investigating its potential as an effective antioxidant and its protective mechanisms against chronic ammonia stress in crucian carp is highly valuable. Experimental fish (initial weight 20.47 ± 1.68 g) were fed diets supplemented with or without 0.1% α-lipoic acid followed by a chronic ammonia exposure (10 mg/L) for 42 days. The results revealed that chronic ammonia stress affected growth (weight gain rate, specific growth rate, and feed conversion rate), leading to oxidative stress (decreased the activities of antioxidant enzymes catalase, superoxide dismutase, glutathione peroxidase; decreased total antioxidant capacity), increased lipid peroxidation (accumulation of malondialdehyde), immune suppression (decreased contents of nonspecific immune enzymes AKP and ACP, 50% hemolytic complement, and decrease of immunoglobulin M), impaired ammonia metabolism (reduced contents of Glu, GS, GSH, and Gln), imbalance of expression of induced antioxidant-related genes (downregulation of Cu/Zu SOD, CAT, Nrf2, and HO-1; upregulation of GST and Keap1), induction of pro-apoptotic molecules (transcription of BAX, Caspase3, and Caspase9), downregulation of anti-apoptotic gene Bcl-2 expression, and induction of endoplasmic reticulum stress (upregulation of IRE1, PERK, and ATF6 expression). The results suggested that the supplementation of α-lipoic acid could effectively induce humoral immunity, alleviate oxidative stress injury and endoplasmic reticulum stress, and ultimately alleviate liver injury induced by ammonia poisoning (50–60% reduction). This provides theoretical basis for revealing the toxicity of long-term ammonia stress and provides new insights into the anti-ammonia toxicity mechanism of α-lipoic acid.

Chronic ammonia toxicity disturbed energy homeostasis and damaged the hepatopancreas of swimming crab Portunus trituberculatus

Ammonia is toxic to aquatic animals and its chronic effects on the swimming crab Portunus trituberculatus is still not fully understood. Therefore, we conducted this study to detect the responses of energy metabolism of crabs to chronic high environmental ammonia (HEA) exposure by exposing them to HEA (5 and 15 mg·L−1) for 15 d and subsequently recovering in natural seawater for 7 d. Then we analyzed the glucose and lactate content, ATPases activities and the expression of the genes involved in energy homeostasis. Besides, glutamic pyruvic transaminase (GPT), glutamic oxaloacetic transaminase (GOT), alkaline phosphatase (AKP) activity and histological changes were assayed to determine the HEA-induced hepatopancreas damage. Results showed a HEA dose- and exposure time-dependent mortality and hepatopancreas damage. This was accompanied by a loss of energy homeostasis as indicated by the significant increase of AMP/ATP ratio and genes expression involved in AMPK pathway (P < 0.05). While indices such as HMGCR expression, glucose content and ion related ATPases demonstrated the energy dishomeostasis might be related with the inhibitory effect of chronic HEA on energy regulatory capacity especially when HEA approached 15 mg·L−1. In summary, chronic HEA can seriously damage hepatopancreas structure and function of energy metabolism in P. trituberculatus, and this deleterious effect could even not be completely repaired in a short recovery time.

Comparison of immune defense and antioxidant capacity between broodstock and hybrid offspring of juvenile shrimp (Macrobrachium nipponense): Response to acute ammonia stress

Ammonia is a major environmental pollutant in the aquatic system that poses a great threat to the health of shrimp. Macrobrachium nipponense, as one of the large-yield farmed shrimp, is facing germplasm degradation. Genetic improvement through hybridization is one of the effective methods to solve this problem. However, there are few studies on the effects of ammonia nitrogen on the germplasm resources of M.nipponense. In this study, the broodstock populations (Dianshan, DS) and hybrid offspring (DS ♀×CD [Changjiang, CJ ♂×Dongting, DT ♀], SCD) were exposed to 0, 5, or 20mg/L of ammonia for 96h. The survival rate of the SCD group was greater than the DS group, although there were no significant differences in weight gain rate and length gain rate (p>0.05). The number of positive cells and apoptosis rates in the DS group were significantly greater than in the SCD group after ammonia exposure (p<0.05). As the ammonia concentration increased, the antioxidant enzyme activities in the SCD group were significantly higher than DS group, while the hepatotoxicity enzyme activities in the SCD group were significantly lower than DS group (p<0.05). The trends in the expression of antioxidant- and immune-related genes were generally consistent with the activities of antioxidant enzymes. Our study found that the hybrid population had stronger stress resistance than their parent populations at the same ammonia concentration. This study confirms our speculation that hybrid population has a greater advantage in antioxidant immunity, which also provides reference for the follow-up study of chronic ammonia toxicity.

Acute and chronic toxicity of ammonia in Persian sturgeon, Acipenser persicus, fingerlings

In the present study, susceptibility of Persian sturgeon, Acipenser persicus, to un-ionized ammonia (UIA) was studied. Fish with an average weight of 5.52±0.45 g were exposed to different concentrations of un-ionized ammonia (UIA) to determine median lethal concentration (96-h-LC 50 ). The fish were exposed to six different concentrations of UIA (control, 0.16, 0.31, 0.62, 0.94 and 1.25 mg/l UIA). The control group was not challenged with ammonia (0.0008 mg/l UIA). The results showed that the 96-h-LC 50 of UIA in Persian sturgeon was 0.46 mg/l. According to 96-h-LC 50 ,mid-term exposure to sub-lethal UIA was examined. In the chronic examination, the fish were exposed to different levels of sub-lethal ammonia; control (0.0008 mg/l UIA), 10% of LC 50 (0.05 mg/l UIA), 5% of LC 50 (0.025 mg/l UIA) and 1% of LC 50 (0.005 mg/l UIA) for 30 days. Final length, final weight, weight gain, specific growth rate, daily weight gain and body weigh index decreased significantly in the fish exposed to 0.05 and 0.025 mg/l UIA. According to the results, conversion ratio and condition factor indices were higher in the fish exposed to 0.005 mg/l UIA and control group compared with the fish exposed to 0.05 and 0.025 mg/l UIA.

Growth performance, physiological response and histology changes of juvenile blunt snout bream, Megalobrama amblycephala exposed to chronic ammonia

Ammonia is one of the major environmental pollutants in freshwater aquatic systems that affects the survival and growth of organisms. In the present study, a nine-week experiment was conducted to investigate the chronic toxicity of ammonia on survival and selected hematological parameters, antioxidant ability, and histological structure in juvenile Chinese blunt snout bream, Megalobrama amblycephala. Fish were exposed to one of five different ammonia concentrations (0, 5, 10, 15, and 20 mg L −1 total ammonia-N, pH = 7.86 ± 0.41, temperature = 28.23 ± 0.79 °C). Growth performance of fish in the high-ammonia treatment was lower than that of fish in the control group. The survival rate in the group exposed to the highest ammonia-N concentration (20 mg L−1) was significantly lower than that of the control group. The lowest level of white blood cell count (WBC), red blood cell count (RBC), hemoglobin, hematocrit, and plasma glucose and the highest level of plasma ammonia, cortisol and aspartate transaminase were observed in fish exposed to ammonia-N at 20 mg L −1 compared with the control group. The liver superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPX) activities in fish exposure to 20 mg L −1 ammonia-N group were significantly lower than those in the control group, while oxidative stress indices (levels of malondialdehyde, MDA) was significantly higher than those in the control group. Regression analysis found that growth performance, plasma parameters, hematological parameters, and antioxidant status of fish were significant linear correlated to ammonia-N concentration. Fish exposed to various concentrations of ammonia displayed histopathologic alterations in both gill and liver tissue. Furthermore, morphological examination by transmission electron microscopy revealed that gill tissues displayed vacuolation of the cytoplasm, damaged mitochondria, increased heterochromatin, and intense desquamation of pavement epithelial cells on the gill lamellae. Our findings suggest that the stress responses induced in juvenile blunt snout bream by chronic exposure to ammonia are not limited to simple growth inhibition, but are accompanied by changes in oxidative stress, plasma parameter effects, and alterations in the histology of the liver and gill. Blunt snout bream had a dose-dependent effect on ammonia-N. We preliminarily suggest that the level of plasma ammonia, MDA, CAT, AST, FER, and SGR can be used as an indicator for chronic ammonia-N toxicity, but further research and verification are needed in the future.

Chronic ammonia toxicity to juveniles of 2 tropical Australian freshwater mussels (Velesunio spp.): Toxicity test optimization and implications for water quality guideline values.

Freshwater mussels play key roles in aquatic ecosystems, but are experiencing a global decline. Although studies have reported high acute sensitivity of mussels to some contaminants, chronic toxicity data are lacking for deriving high-reliability water quality guideline values. Ammonia is a contaminant of potential concern in some catchments of tropical northern Australia, where freshwater mussels are important ecological and cultural components. The extremely soft waters (hardness < 5 mg/L) of these environments can result in increased toxicity of many contaminants including ammonia, and regionally relevant tropical guideline values are needed to adequately protect these unique ecosystems. An optimized 14-d toxicity test protocol was used to assess the chronic toxicity of ammonia for 2 species, the lotic Velesunio sp. and the lentic Velesunio angasi. Ammonia exposures were conducted at pH 6.0 and 27 ± 0.5 °C to represent local environmental conditions, using shell length growth rate as the endpoint. Chronic toxicity estimates indicated high sensitivity to ammonia, with mean median effect concentrations (in total ammonia nitrogen) being 7.0 mg/L for V. angasi from the semi-urbanized Lake Bennett, 9.2 mg/L for V. angasi from Sandy Billabong, and 11.3 mg/L for Velesunio sp. from Gulungul Creek. When the 10% effect concentration values were compared with other chronic ammonia data (normalized to pH 7.0 and 20 °C), Velesunio spp. were found to be more sensitive than 8 of 16 other temperate and 7 of 9 tropical invertebrate and fish species. These chronic toxicity estimates will be used to further inform regionally relevant and site-specific guideline values. Environ Toxicol Chem 2019;38:841-851. © 2019 Commonwealth of Australia. Published by Wiley Periodicals Inc. on behalf of SETAC.

Biomarkers as tools to assess the chronic toxicity of ammonia in the juvenile Mugil cephalus

ABSTRACTWith juvenile fish as the subject, the effects of low concentration ammonia on antioxidant system were studied using Mugil cephalus. Samples of gill and liver tissue were obtained from 0.35, 0.70, 1.5 and 3 mg/L ammonia groups at 0, 5, 10, 15 and 20 days of exposure, at which times the biomarkers were measured. Results showed that gill malondialdehyde (MDA) content exhibited an initial significant increase (p ≤ 0.05) at unionised ammonia concentrations of 0.70, 1.5 and 3.0 mg/L on day 5, followed by subsequent declines, while liver MDA levels exhibited significant increases (p ≤ 0.05) at unionised ammonia concentrations of 1.5 mg/L starting on day 10 and at 3.0 mg/L starting on day 5. With exposure to ammonia at different concentrations, Na+-K+-ATPase activity in liver and gill decreased over time. The Na+-K+-ATPase activity was negatively related to ammonia concentration from 0.70 to 3.0 mg/L. Overall, our results show that MDA and Na+-K+-ATPase, evaluated here as potential biomarkers of ammonia exposure, exhibited responses to sublethal concentrations of ammonia that were concentration dependent.

Acute and Chronic Effects of Ammonia on Juvenile Cuttlefish, Sepia pharaonis

AbstractThe aim of this study was to provide a reference value for the safe regulation and control of ammonia nitrogen in the aquaculture of Sepia pharaonis. The effects of acute and chronic toxicity of ammonia on the cuttlefish, S. pharaonis, were tested experimentally using juvenile S. pharaonis. The results showed that the half‐lethal concentration (LC50 ) values of ammonia nitrogen in juvenile S. pharaonis with a body weight of 6.52 ± 0. 23 g at 24, 48, 72, and 96 h were 31.72, 25.77, 23.33, and 18.33 mg/L, respectively, and the corresponding un‐ionized ammonia nitrogen (UIA‐N) concentrations were 1.66, 1.35, 1.22, and 0.96 mg/L, respectively. Compared with the control, the survival rate, specific growth rate, and feed intake of juvenile S. pharaonis declined significantly, and the feed conversion ratio and hepatosomatic index increased significantly at 56 d after exposure to &gt;1 mg/L ammonia nitrogen. Juvenile S. pharaonis should be maintained at a concentration of ammonia nitrogen of no more than 1 mg/L (UIA‐N is 0.056 mg/L) in culture, and removing harmful nitrogenous wastes from the seawater is critical in maintaining cuttlefish culture.

Growth, oxidative stress responses, and gene transcription of juvenile bighead carp (Hypophthalmichthys nobilis) under chronic-term exposure of ammonia.

Ammonia toxicity has become a universal problem for aquatic animals, especially fish. The purpose of the present study was to assess the chronic toxicity of ammonia to the juvenile bighead carp (Hypophthalmichthys nobilis). The authors measured the responses of growth performance (specific growth rate, condition factor, body weight, and body length), oxidative stress, and related gene transcription of juvenile bighead carp exposed to solutions with different concentrations of un-ionized ammonia (UIA; 0 mg L(-1) , 0.053 mg L(-1) , 0.106 mg L(-1) , 0.159 mg L(-1) , and 0.212 mg L(-1) ). The results showed that UIA had no effect on growth performance, glutathione content, or glutathione S-transferase gene transcription, but superoxide dismutase (SOD) activity was significantly elevated. In addition, different concentrations of UIA produced different degrees of damage to juvenile bighead carp: compared with control, lower UIA levels significantly decreased gene transcription of catalase (CAT) and increased malondialdehyde (MDA) levels; higher UIA concentration (0.212 mg L(-1) ) significantly increased gene transcription of the antioxidant enzymes CAT and SOD and reduced MDA levels. The data clearly demonstrate that chronic exposure of UIA at lower concentrations can result in some degree of impairment of antioxidative function, and chronic exposure at higher concentrations can enhance damage to juvenile bighead carp by modulating antioxidant enzyme activities and gene transcription.

Changes in the selected hematological parameters and gill Na +/K + ATPase activity of juvenile crucian carp Carassius auratus during elevated ammonia exposure and the post-exposure recovery

The increase in concentration of ammonia in lake water during the degradation of algal blooms may last for several weeks and thus cause chronic toxicity to aquatic organisms. The purpose of this study was to assess the chronic toxicity of ammonia on the selected hematological parameters and gill Na +/K + ATPase activity of juvenile crucian carp Carassius auratus during elevated ammonia exposure and the post-exposure recovery. Juvenile crucian carp were exposed in different ammonia solutions for 45 days and then immediately transferred to pristine freshwater to initiate a 15-day recovery period. Results showed sub-lethal ammonia significantly deters growth and a 15-day recovery period was not sufficient for the fish to compensate for the loss of growth. The fish exhibited a continuous decrease in red blood cell (RBC), the total hemoglobin (Hb), and gill Na +/K + ATPase activity as the concentration of NH 3-N increased. After the 15-day recovery period, RBC, Hb, and gill Na +/K + ATPase activity had recovered to similar levels as the controls.

Acute and chronic toxicity of ammonia, nitrite, and nitrate to the endangered topeka shiner (Notropis topeka) and fathead minnows (Pimephales promelas)

Toxicity tests with ammonia, nitrite, and nitrate were conducted on the endangered Topeka shiner (Notropis topeka) to determine if current U.S. Environmental Protection Agency (U.S. EPA) water quality criteria are protective of this species. Results from acute lethal and chronic growth tests are reported for both Topeka shiners and fathead minnows (Pimephales promelas). Embryo-larval tests were conducted with only fathead minnows because Topeka shiner embryos were not available. Predicted outcomes for Topeka shiner embryo-larval toxicity endpoints were calculated by comparing relationships between growth tests and embryo-larval tests for fathead minnows and extrapolating those relationships to Topeka shiners. Results show that the U.S. EPA's criterion for total ammonia-nitrogen (TAN), 1.24 mg/L when early life stages are present, would be protective, given that our most sensitive result was a predicted maximum acceptable toxicant concentration (MATC) for Topeka shiners at 5.63 mg/L TAN, calculated from the fathead minnow chronic embryo-larval test. The U.S. EPA's criterion for nitrite (5 mg/L) would not be protective, given that our most sensitive result was a predicted MATC for Topeka shiners of 3.97 mg/L NO2-N, calculated from the fathead minnow chronic embryo-larval test. However, nitrite is generally transient, and unpublished field data show levels far lower than the criterion. Finally, the U.S. EPA's recommendation of a maximum of 90 mg/L NO3-N for the protection of warmwater fishes would protect Topeka shiners but not fathead minnows. For Topeka shiners, the MATC from the 30-d juvenile growth test was 360 mg/L NO3-N, but for fathead minnows, the MATC was 84 mg/L. More field sampling may be needed to determine if levels comply with criteria, especially in Topeka shiner critical habitat.

Chronic Toxicity of Ammonia to Early Life Stage Rainbow Trout

AbstractA 90‐d ammonia toxicity test for early life stage rainbow trout Oncorhynchus mykiss was conducted using newly fertilized eggs from a wild strain of fish. The toxicity test was conducted at a pH of 7.75 and temperature of 11.4°C. Hatch success and survival of sac fry were not affected by ammonia exposure. Survival, growth, and biomass of swim‐up fry were significantly reduced at an ammonia‐nitrogen (NH3‐N) concentration of 16.8 mg NH3‐N/L of water but were unaffected by exposures to 7.44 mg NH3‐N/L or lower concentrations. The chronic toxicity value was 11.2 mg NH3‐N/L, and the EC20 (concentration estimated to cause a 20% reduction in organism performance compared with the control) based on biomass at test termination was 7.72 mg NH3‐N/L. Development of sac fry to the swim‐up stage was retarded by ammonia, but fry exposed to 7.44 mg NH3‐N/L or lower concentrations appeared to recover by the end of the test. Histological analysis of the gills of exposed fry did not detect any gill pathology. U.S. Environmental Protection Agency chronic ammonia criteria are protective of early life stages of rainbow trout under test conditions.

The effects of acute and chronic ammonia exposure during early life stages of the gulf toadfish, Opsanus beta

The gulf toadfish ( Opsanus beta) is unusual among teleosts in that it is facultatively ureotelic and adults and juveniles have a particularly high tolerance to environmental ammonia. Male toadfish brood their offspring in confined nests. It has been hypothesized that the potential accumulation of ammonia in nests from the male and the offspring, coupled with suspected low ammonia tolerance in offspring would provide the selective pressure necessary for excretion of the less toxic urea by adult toadfish. This study examines this so-called ‘nest-fouling’ hypothesis through acute and chronic ammonia toxicity testing on early life stages of O. beta. In addition, nitrogen elimination was examined among embryos, yolk-sac larvae and juveniles where we found an ontogenic shift from ammonotely to ureotely with advancing life history stages. The acute ammonia 96 h LC 50 values for embryos and larvae were 63.6 and 5.45 mmol-N l −1 total ammonia ( T Amm), respectively. Thus, these early life stages are more tolerant to ammonia than either juveniles or adults and LC 50 values are at least 2 orders of magnitude greater than concentrations naturally occurring at nest sites. Furthermore, 40 days exposures at mean and maximum NH 3 concentrations normally found within nests revealed no observable detrimental effects. In fact, growth in terms of wet or dry weight was greatest at the maximum NH 3 concentration. We therefore conclude that the nest-fouling hypothesis is not a viable explanation for ureotely in the gulf toadfish.

Acute and Chronic Toxicity of Ammonia to the Amphipod Hyalella azteca under Hard Water Conditions

Acute and Chronic Toxicity of Ammonia to the Amphipod Hyalella azteca under Hard Water Conditions

Chronic Toxicity of Ammonia to New Zealand Freshwater Invertebrates: A Mesocosm Study.

Freshwater macroinvertebrate communities were established within 12 artificial streams or "toroidal" mesocosms and exposed to three replicated concentrations of ammonia for 29 days at constant temperature (16 degrees C) and pH (median 8.4). The criterion units (CU = measured [ammonia]/US EPA 1985 chronic criterion value) of total ammonia in the LOW, MED, and HIGH treatments were 2.0, 4.8, and 13 CUs respectively, and 1.9, 5.8, and 12 CUs for the unionized ammonia. Macroinvertebrates were tolerant of the ammonia exposures with no significant (p > 0.1) effect on taxa richness; number of taxa in the orders Ephemeroptera, Plecoptera, and Trichoptera (EPT); or the quantitative macroinvertebrate community index (QMCI), a biotic index proposed for assessing effects of organic enrichment in New Zealand streams. Significant differences (p < 0.05) occurred for the mean abundance and the numbers of EPT individuals (QEPT), with the HIGH treatment significantly lower (-41%) than the control for both abundance and QEPT. Of the major species, only the mayflies Deleatidium sp. (Ephemeroptera: Leptophlebiidae) and Coloburiscus humeralis (Ephemeroptera: Oligoneuriidae) showed significant reductions in abundance, with only the caddisflies Beraeoptera roria (Trichoptera: Conoesucidae) and Confluens sp. (Trichoptera: Conoesucidae) showing significant increases in abundance. The abundance of juvenile Deleatidium sp. had a negative concentration-response relationship that resulted in an 82% decrease in abundance in the HIGH treatment. Drift of invertebrates showed no response to ammonia treatments. The 29-day EC(50) values for Deleatidium sp. for total and unionized ammonia were 2.15 mg (N)/L (pH 8.4) and 0.145 mg (NH(3)-N)/L. No observed effect concentration (NOEC) values were 0.95 mg (N)/L and 0.066 mg (NH(3)-N)/L, and the threshold effect concentration (TEC) was 1.49 mg (N)/L and 0.102 mg (NH(3)-N)/L. Comparison of the Deleatidium sp. chronic ammonia sensitivity data with the US EPA 1985 chronic criterion value (CCC = 0.45 mg [N]/L, pH 8.4, 16 degrees C) showed the TEC value for total ammonia was 3.3x CCC, and 2.2x higher than the updated US EPA 1998 criteria. The findings suggest that use of the US EPA criteria would provide minimal protection for Deleatidium for chronic ammonia exposure, and that development of site-specific criteria, covering a wide range of environmental conditions, may be required to adequately protect this species.http://link.springer-ny.com/link/service/journals/00244/bibs/37n3p338.html

Chronic toxicity of ammonia to the amphipod Hyalella azteca; Importance of ammonium ion and water hardness

Ammonia toxicity resulted in the continuous mortality of Hyalella azteca for up to 10 weeks with similar mortality rates for adults and young. Growth was not reduced at concentrations below those causing chronic mortality (1 mM total ammonia in Lake Ontario water), but reproduction was reduced at concentrations as low as 0·32 mM. Chronic mortality was a function of total ammonia (or ammonium ion), and not un-ionized ammonia, when the pH was adjusted by addition of acid. However, a 1 in 10 dilution of Lake Ontario water in distilled water resulted in a 10-fold reduction in the 4 week LC50. In contrast to common practice, ammonia toxicity to Hyalella is best defined on a total ammonia basis, but variations in hardness and other ions must be taken into account.

Chronic toxicity of ammonia to juvenile gilthead seabream Sparus aurata and related histopathological effects

Chronic toxicity of ammonia to juvenile gilthead seabream Sparus aurata and related histopathological effects

Chronic toxicity of ammonia to juvenile gilthead seabream Sparus aurata and related histopathological effects

Effect of 20 days exposure of juvenile gilthead seabream (Sparus aurata) to elevated levels of ammonia on growth and survival was examined in a continuous flow system. Suppressed growth and reduced survival were observed at concentrations of 8.2 and 13 mg l−1 total ammonia‐N (0.5 and 0.7 mg l−1 un‐ionized ammonia‐N, respectively) and higher. The maximum acceptable toxic concentration (MATC) for growth was between 4.8 to 8.2 mg l−1 total ammonia‐N (0.3 and 0.5 mg l−1 un‐ionized ammonia‐N, respectively). Fish exposed to high ammonia levels (13 mg l−1 total ammonia‐N, 0.7 mg l−1 un‐ionized ammonia‐N) displayed clear signs of liver pathology. Existing evidence suggests that S. aurata is less sensitive to ammonia than other reported marine and freshwater fish.Under certain conditions ammonia concentration in the intensive fish ponds in Eilat may exceed the no observed effect concentration for S. aurata.

Acute and chronic toxicity of ammonia to juvenile Metapenaeus macleayi and Penaeus monodon and the influence of low dissolved-oxygen levels

Acute toxicity of ammonia was estimated as 96-h LC 50 values. For juvenile school prawns, Metapenaeus macleayi, and leader prawns, Penaeus monodon, these were 1.39 and 1.69 mg un-ionised ammonia, NH 3-N/l (26.3 and 37.4 mg total ammonia-N/l), respectively. Reduced dissolved-oxygen (DO) levels significantly ( P<0.05) increased the acute toxicity of ammonia to P. monodon. Ninety percent of prawns held for 96 h at a DO level of 2.3 mg/l and an ammonia concentration of 1.60 mg NH 3-N/l (33.5 mg total ammonia-N/l) died, whereas only 33.3% died at a DO level of 5.7 mg/l and a similar ammonia concentration of 1.63 mg NH 3-N/l (33.9 mg total ammonia-N/l). The “maximum acceptable” level of ammonia was defined as that which reduced growth by 5% over 3 weeks. For M. macleayi and P. monodon these levels were 0.35 and 0.21 mg NH 3-N/l (7.7 and 4.1 mg total ammonia-N/l), respectively.

The acute and chronic toxicity of ammonia to marine fish and a mysid

The acute toxicity (96-hr LC50) of un-ionized ammonia to mysids (Mysidopsis bahia) and larval inland silversides (Menidia beryllina) was influenced by pH and salinity in a species specific manner. With mysids, NH3 was most toxic at pH 7.0 and less toxic at pH 8.0 and 9.0. In contrast, NH3 toxicity to inland silversides was greatest at pH 7.0 and 9.0 and lowest at pH 8.0. A drop in salinity from 31 g/kg to 11 g/kg uniformly increased toxicity to mysids over this pH range. In contrast, in silversides at 11 g/kg, NH3 toxicity was less at pH 7.0, greater at pH 8, and slightly less at pH 9, relative to the toxicity at 31 g/kg. Temperature had no significant effect on the acute toxicity of un-ionized ammonia with acclimated mysids tested at 18, 25 and 32.5 degrees C, but did have a small effect with acclimated larval sheepshead minnows (Cyprinodon variegatus) tested at 13, 25 and 32.5 degrees C. The chronic toxicity value (the geometric mean of the highest no-effect concentration and lowest effect concentration) at pH 8.0, 25 degrees C and 31 g/kg salinity is 0.061 mg NH3/L for inland silversides and 0.232 mg NH3/L for mysids; the acute:chronic ratio is 21.3 and 7.2, respectively.