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The effects of feeding and stress on ammonia toxicity in rainbow trout

University of British Columbia

The effect of ammonia on aquatic organisms is an area that has been well studied. Results from various types of toxicity tests, including chronic and acute tests, have been used to establish the water ammonia standards for protection of aquatic life. Tests often follow standard protocols and are conducted under static conditions on unfed and unstressed animals. These conditions are in fact ones when fish are least susceptible to ammonia toxicity since feeding and stress cause increased internal ammonia production. This thesis had two goals. The first determined whether feeding or stress exacerbated ammonia toxicity to a level where standards promulgated by the US EPA were no longer protective for rainbow trout. In this regard, it was determined, using 96-h LC₅₀ tests that present standards did protect rainbow trout that were either feeding, or stressed by high-density conditions. Feeding decreased ammonia toxicity during the first 24-h of ammonia exposure, increasing the LC₅₀ concentration by 30 mg N/L. In contrast, both exposure to stress and Cortisol injections exacerbated ammonia toxicity in fish. The second purpose of this research was to determine the physiological consequences of feeding and stress in rainbow trout exposed to sub-lethal ammonia concentrations. Results from experiments where fish were exposed to 10 mg N /L for 48-h and then terminally sampled for measurement of plasma ammonia, metabolites (glutamate and glutamine) and enzyme activities (glutaminase, glutamine synthetase-GSase, glutamate dehydrogenase-GDH, alanine aminotransferase and aspartate aminotransferase) in brain, liver and muscle tissue, indicated that protection from ammonia toxicity is evoked in feeding fish because glutamine synthetase is upregulated and a-ketoglutarate is likely not limiting the formation of glutamate and glutamine. The non-toxic glutamine is accumulated in the brain, liver and muscle tissue, thus removing ammonia from circulation. The same experiments conducted on fasted fish exposed to stressors (high-density, air-exposure and 3 ppm ambient Cortisol) and then exposed to ammonia showed a different response. These fish were not able to regulate internal ammonia when ammonia exposure commenced and the down-regulation of GSase and glutaminase and up-regulation of GDH indicated that this was likely due to a limitation in a-ketoglutarate available for glutamate formation. Based on two models formulated from the present studies, glutamate regulation is critical in preventing ammonia toxicity.

Thesis/Dissertation

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2009-09-29

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http://hdl.handle.net/2429/13319

Zoology

University of British Columbia

UBCV

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