Transition metals (i.e. copper, zinc, iron, cobalt, selenium, manganese) are essential for the health of most organisms, forming integral components of proteins involved in all aspects of biological function. Their ubiquity is governed by their ability to form a wide range of coordination geometries and redox states, which allows these elements to interact with many cellular entities, performing pivotal roles in cellular respiration, oxygen transport, protein stability, free radical scavenging, and the action of many cellular enzymes, as well as for DNA transcription. However, in excess they are toxic, binding to inappropriate biologically sensitive molecules or forming dangerous free radicals. Consequently, there is a fine balance between metal deficiency and surplus and it is vital for organisms to maintain metal homeostasis via balancing absorption and excretion.Fish are unique among the vertebrates, a consequence of having two routes of metal acquisition, from the diet and from the water. This review will focus on the uptake processes present in the gill and intestinal epithelium of teleost fish for the three most abundant nutritive metals: iron, copper and zinc. The majority of the available literature concerns metal uptake processes in freshwater teleosts, but where appropriate examples exist, information on seawater teleosts will be reviewed. Molecular evidence indicates that transporters for these metals identified in yeast, plants or mammals all show high sequence homology in key functional regions ), but to date, none of these transporters have been characterised in fish. However, due to the evolutionary conservation of these proteins between yeast, plants and mammals, it is envisaged that fish metal transporters will also belong to the large iron, copper or zinc metal transporter protein families already identified. This review will combine physiological and molecular data to provide an overview of metal uptake mechanisms in teleost fish. IronIron is an essential nutrient to almost all organisms. Iron positioning in the haem moiety of haemoglobin increases oxygen binding and carrying capacity, enabling oxygen transfer to all tissues in multicellular organisms. One of iron's key cellular functions is to confer redox activity to the cytochromes involved in respiration, due to its ability to exchange electrons in aerobic conditions. A negative consequence of iron's redox flexibility is that it produces oxygen free radicals that are toxic to the cell. Consequently, in excess, iron can be detrimental to health. In addition, excess waterborne iron may be toxic to fish, due to the formation of iron 'flocs' on the gills, resulting in gill clogging and respiratory perturbations (Peuranen et al., 1994;Dalzell and MacFarlane, 1999). Teleost fish iron homeostasisThe iron content of fish is, in general, considerably lower than that of other vertebrates (Van Dijk et al., 1975), but the precise daily iron requirements for fish are at present unknown. 11The Journal of Experimental Biology 206, 11-23 © 2003 The Compa...

Field trials in Europe with Miscanthus over the past 25 years have demonstrated that interspecies hybrids such as M. 9 giganteus (M 9 g) combine both high yield potentials and low inputs in a wide range of soils and climates. Miscanthus hybrids are expected to play a major role in the provision of perennial lignocellulosic biomass across much of Europe as part of a lower carbon economy. However, even with favourable policies in some European countries, uptake has been slow. M 9 g, as a sterile clone, can only be propagated vegetatively, which leads to high establishment costs and low multiplication rates. Consequently, a decade ago, a strategic decision to develop rapidly multiplied seeded hybrids was taken. To make progress on this goal, we have (1) harnessed Correspondence: John Clifton-

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SUMMARY Ammonia and urea are the primary forms of nitrogen excretion in teleost fish. There exists, however, a discrepancy between the sum of ammonia plus urea nitrogen and total nitrogen, indicating that `unknown' nitrogen end products may play an important role in nitrogen metabolism. The current study analysed a wide range of nitrogen end products in both fed and fasted juvenile rainbow trout. Ammonia-N (53–68%) and urea-N (6–10%) were confirmed as the most important forms of nitrogenous waste, but an interesting finding was the considerable excretion of nitrogen as amino acids(4–10%), via the gills, and as protein (3–11%), probably via the body mucus. Use of anal sutures delineated an important role for the gastrointestinal tract in the production of ammonia-N and urea-N in fed fish, but amino acid-N and protein-N output by this route were both negligible. Alternative nitrogen products – trimethylamine,trimethylamine oxide, uric acid, and nitrite + nitrate – were not excreted in detectable quantities. Creatine-N and creatinine-N outputs were detected but contributed only a small fraction to total nitrogen excretion(<1.4%). Despite the wide scope of nitrogenous end products investigated, a considerable proportion (12–20%) of nitrogen excretion remains unknown. Possible alternative end products and methodological considerations are proposed to explain this phenomenon. The findings described above were used to recalculate the nitrogen quotient(NQ=ṀN/ṀO2)on trout that had been either fasted or fed various daily rations (1%, 3% or 5% dry food per unit wet body mass per day). Feeding increased oxygen consumption (ṀO2)and total-N excretion (ṀN). The NQ is often used as a measure of protein utilisation in aerobic metabolism and assumes that all protein (and amino acid) fuels are converted by oxidation to nitrogenous waste products that are excreted. However, the results showed that calculation of the NQ based on total nitrogen excretion may overestimate protein utilisation in aerobic metabolism because of significant excretion of N in the form of proteins and amino acids, whereas the use of summed ammonia-N and urea-N excretion probably underestimates the contribution of protein towards aerobic metabolism. These errors increase as ration increases, because the discrepancy between total-N excretion and ammonia-N + urea-N excretion increases.