Effects of Environmental pH and Calcium on Ammonia Toxicity in Channel Catfish

Abstract

The twenty-four-hour median lethal concentrations (24-hour LC50) of total ammonia nitrogen (TA-N) to channel catfish (lctalurus punctatus) at pH 7, 8, and 9 (total hardness, 40 rag/liter; temperature, 21-25 C) were 263.6 -+ 11.3 (SE), 38.8 -+ 1.8, and 4.5 -+ 0.2 rag/liter, respectively. The 24-hour LC50 of un-ionized ammonia nitrogen (UIA-N) concentration at pH 8 was significantly higher (1.82 -+ 0.06 mg/liter) than at pH 7 or 9 (1.39 -+ 0.06 and 1.49 -+ 0.12 mg/liter). Enrichment of the water to 440 mg/liter total hardness at pH 7 significantly increased the 24hour LC50 of TA-N and UIA-N (356.3 -+ 16.4 and 1.79 -+ 0.07). Fish exposed to 25 mg/liter TA-N for 12 hours at pH 7 and 8 showed no differences from control fish in hematocrit, percent total plasma protein• or plasma and muscle chloride. Plasma sodium showed no difference between control and experimental groups at pH 7; however, a significant decrease occurred in fish exposed to 25 mg/liter TA-N at pH 8. No differences in blood pH were found between the control groups and fish exposed to 100 and 200 mg/liter TA-N at pH 7, and to 10 and 25 mg/ liter TA-N at pH 8. Plasma sodium depletion is suggested as a contributing mechanism of ammonia toxicity.The principal nitrogenous compound excreted by fish is ammonia, which may reach concentrations that are detrimental to fish and reduce productivity during high density fish culture. Ammonia toxicity has been primarily attributed to the un-ionized form, with the ion-

Morphological changes in the gills of Lophiosilurus alexandri exposed to un‐ionized ammonia

“…It is known that ammonia produces a toxic effect in temperate fishes (Tomasso et al, 1980;Thurston et al, 1984;Peters et al, 1984). In tropical fish species, with potential for aquaculture, studies on lethal concentration of ammonia in fish have been initiated (Ostrensky & Brugger, 1992).…”

“…Ammonia is a common pollutant of natural aquatic systems and constitutes the main nitrogenous waste compound (Tomasso et al, 1980). It is produced mainly in the fish liver (Goldstein et al, 1982), reaches the gills through the blood (Evans & More, 1988), and is excreted in the epithelium by a variety of means (Evans & Cameron, 1986) and then it is transferred to the water.…”

Dissolved oxygen and ammonia levels in water that affect plasma ionic content and gallbladder bile in silver catfish

“…The main process of ammonia excretion in freshwater fish is by the passive transcellular diffusion of NH 3 down a concentration gradient (WRIGHT & WOOD, 1985;RANDALL & WRIGHT, 1987;CLAIBORNE & EVANS, 1988). Exposure to high waterborne NH 3 levels reduced plasma Na + in channel catfish (Ictalurus punctatus) (TOMASSO et al, 1980) and in rainbow trout (Oncorhynchus mykiss), and also increased Na + efflux in rainbow trout (TWITCHEN & EDDY, 1994). However, it did not change plasma ion levels in other experiments (WILSON & TAYLOR, 1992;VEDEL et al, 1998).…”

Assessment of Dredged Material Toxicity in San Francisco Bay

“…Exposures of teleosts to elevated environmental levels of ammonia have been found to result in degenerative gill and kidney damage (Burrows 1964, Smart 1976, Thurston et al 1978, reduced growth rates (Burrows 1964, Colt and Tchobanoglous 1978, Robinette 1976, reduced 02 carrying capacity of the hemoglobin (Sousa and Meade 1977), increased urine output (Lloyd and Orr 1969) and the release of corticosteroid hormones (Tomasso et al 1980). Additional research has indicated low dissolved oxygen enhances the toxicity of ammonia (Merkens and Downing 1957, Thurston et al 1981a, Lloyd 1961).…”