SUMMARY
The present study investigated the role of ammonia as a trigger for hatching, mechanisms of ammonia detoxification and the localization of urea cycle enzymes in the early life stages of freshwater rainbow trout (Oncorhynchus mykiss). The key urea cycle enzyme carbamoyl phosphate synthetase III was found exclusively in the embryonic body (non-hepatic tissues); related enzymes were distributed between the liver and embryonic body. ‘Eyed-up’ trout embryos were exposed either acutely (2h) to 10mmoll−1 NH4Cl or chronically (4 days) to 0.2mmoll−1 NH4Cl. Time to hatching was not affected by either acute or chronic NH4Cl exposure. Urea levels, but not ammonia levels in the embryonic tissues, were significantly higher than in controls after both acute and chronic NH4Cl exposure, whereas there were no significant changes in urea cycle enzyme activities. Total amino acid levels in the embryonic tissues were unaltered by chronic ammonia exposure, but levels of most individual amino acids and total amino acid levels in the yolk were significantly lower (by 34–58%) than in non-exposed controls. The data indicate that trout embryos have an efficient system to prevent ammonia accumulation in embryonic tissue, by conversion of ammonia to urea in embryonic tissues and through elevation of ammonia levels in the yolk.
Rainbow trout (Oncorhynchus mykiss) urea cycle and polyamine synthesis gene families show dynamic expression responses to inflammation
