Effects of prolonged exposure to ammonia on the blood and liver glycogen of coho salmon (Oncorhynchus kisutch)

Buckley, James A.; Whitmore, Cecil M.; Liming, Brian D.

doi:10.1016/0306-4492(79)90077-7

Cited by 15 publications

(9 citation statements)

References 42 publications

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“…This author also reported swelling of cells, which would be consistent with the observations on blood from experimental fish from the second test. However, unlike the results from the present study, Buckley et al [32] reported slightly, but significantly, reduced hemoglobin concentrations and hematocrit in coho salmon exposed for 91 d at 0.33 mg NH 3 ‐N/L.…”

Section: Discussioncontrasting

confidence: 99%

Effects of short‐term pulsed ammonia exposure on fish

Milne

Seager

Mallett

et al. 2000

Enviro Toxic and Chemistry

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Abstract-Two series of laboratory experiments were undertaken to investigate the influences of exposure duration and frequency on the toxicity of short-term pulses of ammonia to rainbow trout (Oncorhynchus mykiss Walbaum) and brown trout (Salmo trutta L.). For the investigation of exposure duration, rainbow trout were exposed to a range of unionized ammonia concentrations in single pulses of 1, 6, or 24 h, and mortality was recorded as the endpoint. For the investigation of exposure frequency, brown trout were exposed to repeated sublethal ammonia pulses of different concentrations either once or three times weekly over a period of 53 d to simulate intermittent pollution episodes. A range of endpoints were measured, including growth, gill condition, blood indices, and organ-to-body weight ratios. The results suggest that exposure duration and frequency are both important factors influencing the severity of effect in fish exposed to short-term ammonia peaks. Growth, gill condition, organ weights, and hematocrit were all significantly affected by repeated exposures, particularly at the higher exposure frequency. The results of this study confirm that the duration and return period of transient pollution events are critical dimensions when considering the development of environmental quality standards for intermittent pollution.

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Section: Discussioncontrasting

confidence: 99%

Effects of short‐term pulsed ammonia exposure on fish

Milne

Seager

Mallett

et al. 2000

Enviro Toxic and Chemistry

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“…Respiratory impairment in fish resulting from exposure to ammonia-N was also studied (Smart 1978; Buckley et al 1979), and it was concluded that oxygen consumption generally increases when fish are acutely exposed to ammonia-N. Both oxygen uptake and ammonia-N excretion of P. juponicus increased with decreasing salinity and increased directly with previous ammonia-N concentration (Chen and Chen 1997).…”

Section: Discussionmentioning

confidence: 98%

Acute toxicity of ammonia on juvenile cobia (Rachycentron canadum, Linnaeus, 1766) according to the salinity

Barbieri

Doi

2011

Aquacult Int

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Juvenile cobia (Rachycentron canadum) (total length 15.16 ± 0.92 cm and weight 19.26 ± 4.5 g) were exposed to different concentrations of ammonia-N (unionized plus ionized ammonia as nitrogen), using the static renewal method at different salinity levels of 5, 20, and 35% at pH 8.1 and 25°C. The 24, 48, 72, 96 h LC 50 values of ammonia-N for R. canadum juveniles were 60.mg l -1 at 5%, respectively. The 24, 48, 72, 96 h LC 50 values of NH 3 -N (unionized ammonia as nitrogen) were 1.81, 1.46, 1.12, and 0.68 mg l -1 at 35%; 1.75, 1.49, 0.96, and 0.65 mg l -1 at 20%; and 1.52, 0.97, 0.71, and 0.31 mg l -1 at 5%, respectively. As the salinity decreased from 35 to 5%, susceptibility of ammonia-N increased by 34.5, 47.88, 50.56, and 64.23% after 24, 48, 72, and 96 h exposure, respectively. Furthermore, we found that exposure of fish to ammonia-N caused an increase in oxygen consumption of 129.1, 157.5, and 192% and a decrease in the ammonia excretion level of 53.4, 38.2, and 23.3% with respect to the control.

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“…The gradual disappearance of obvious clinical signs in our fish, starting at about 3 weeks, suggested re-establishment of normal blood ammonia levels through homeostatic control mechanisms such as increased excretion or detoxifying reactions. Buckley, Whitmore & Liming (1979) found no change in blood level of total ammonia in freshwater coho salmon, O. kisutch (Walbaum), after 91 days of exposure to un-ionized ammonia levels of up to 0-27 mg/1, but they observed increased plasma sodium levels and suggested that this was the result of an exchange of NH4+ for external Na+ across the branchial epithelium.…”

Section: Discussionmentioning

confidence: 97%

The pathology of chronic ammonia toxicity in rainbow trout, Salmo gairdneri Richardson

Daoust

Ferguson

1984

Journal of Fish Diseases

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Two groups of rainbow trout fingerlings were exposed for 90 days to 0-2 and 0-4 mg/I of un-ionized ammonia, respectively. Several fish exposed to the higher concentration soon developed clinical signs suggestive of a neurological dysfunction but subsequently recovered. No lesion attributable to ammonia was seen in the gills of any of the fish. This raises questions about the precise role of ammonia in the production of gill diseases in intensively cultured trout.

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Effects of prolonged exposure to ammonia on the blood and liver glycogen of coho salmon (Oncorhynchus kisutch)

Cited by 15 publications

References 42 publications

Effects of short‐term pulsed ammonia exposure on fish

Effects of short‐term pulsed ammonia exposure on fish

Acute toxicity of ammonia on juvenile cobia (Rachycentron canadum, Linnaeus, 1766) according to the salinity

The pathology of chronic ammonia toxicity in rainbow trout, Salmo gairdneri Richardson

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