Nitrogen metabolism and excretion in fish: integration from behaviour to genes

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All animals produce waste nitrogen as ammonia when they digest a meal, or in the normal maintenance of body protein. Ammonia is toxic to the nervous system, and as little as a doubling of blood ammonia levels in humans (e.g., as might be seen in liver or kidney disease) can eventually lead to coma and death. Therefore, all animals must either excrete ammonia directly (to the water as is possible in aquatic animals) or detoxify it to a less toxic compound for excretion in a more concentrated form (e.g., urea, as in many terrestrial animals, including humans). It was once thought that the genes for urea production in aquatic species like fish were not expressed because they were not needed in an aquatic environment where direct excretion of ammonia predominates. However, research in recent decades has shown that these genes are in fact needed in (probably most) embryonic fish, and are also used rarely by some species of fish as adults. The proposed research examines one such family of fishes, the toadfish and midshipmen, that contains selected members that make and excrete urea as a nitrogenous waste product. The group will be used to study a novel hypothesis that urea is use to 'cloak' the scent of toadfish to potential predators. The precise mechanisms in the gastrointestinal tract, gills and nervous system that allow toadfish to control urea excretion in discrete pulses will be examined. Furthermore, the action of several key genes involved in transport and metabolism of urea and ammonia will be studied, including the so-called Rhesus proteins (which in humans are responsible for the "Rh factors" important in blood transfusions). The research may eventually have application in fish aquaculture.