title: Exposure of brown trout Salmo trutta to a sublethal concentration of copper in soft acidic water: effects upon gas exchange and ammonia accumulation.
abstract: The present study was undertaken to answer two questions relating to the exposure of brown trout Salmo trutta to sublethal concentrations of copper and low pH (CLP) for 96 h. (1) What is the effect of these pollutants on the rate of oxygen consumption (M(O(2))) at different levels of exercise and (2) why does ammonia accumulate within these fish, when the low external pH should favour the diffusion of NH(3) across the gills? Mean M(O(2)) of fish in CLP and control (normal pH and no added copper) conditions were not significantly different from each other at any level of exercise. This suggests that exposure to CLP was not a 'loading' factor at any level of activity. However, both maximum M(O(2)) and critical swimming speed (U(crit)) were significantly lower in the CLP trout (5.5+/-1.6 mmol O(2) kg(-1) h(-1) and 1.12+/-0.06 BL s(-1), respectively) than in control fish (18.5+/-2.3 mmol O(2) kg(-1) h(-1) and 2.04+/-0.11 BL s(-1), respectively). There was no evidence from cardiovascular variables, such as heart rate and cardiac output, to suggest any changes in the oxygen transport system to compensate for any possible reduction in branchial gas exchange. Thus, it is suggested that oxygen exchange and transport do not limit the swimming performance of CLP trout, but that exposure to CLP reduces the maximum demand for O(2), i.e. it is a limiting factor. The accumulation of ammonia in the plasma and white muscles during exposure to CLP has already been implicated in reducing the swimming performance of brown trout. Inhibition of cortisol synthesis abolished a large proportion of the increases in both the accumulation and excretion of ammonia that occurred during the second 48 h of the exposure to CLP, but did not inhibit ammonia accumulation completely. It is suggested that CLP not only causes an increase in the rate of production of ammonia, which is enhanced when the level of cortisol starts to increase after 48 h, but that it also inhibits an excretory mechanism (most probably Na(+)/NH(4)(+) exchange) that is non-obligatory under 'normal' conditions (when passive diffusion is sufficient), but is required in order to respond to unusually high ammonia loads.
authors.affiliation: School of Biosciences, The University of Birmingham, Edgbaston, Birmingham B15 2TT, UK.
authors.forename: M W
authors.initials: MW
authors.lastname: Beaumont
authors.forename: P J
authors.initials: PJ
authors.lastname: Butler
authors.forename: E W
authors.initials: EW
authors.lastname: Taylor
mesh_terms: D000641:Ammonia / Q000378:metabolism; D000818:Animals; D002320:Cardiovascular Physiological Phenomena; D002319:Cardiovascular System / Q000187:drug effects; D003300:Copper / Q000633:toxicity*; D005880:Gills / Q000187:drug effects / Q000378:metabolism; D006854:Hydrocortisone / Q000037:antagonists & inhibitors / Q000378:metabolism; D006863:Hydrogen-Ion Concentration; D008797:Metyrapone / Q000494:pharmacology; D010101:Oxygen Consumption / Q000187:drug effects; D013550:Swimming; D014337:Trout / Q000378:metabolism* / Q000502:physiology
chemical_list: D000641:Ammonia; D003300:Copper; D006854:Hydrocortisone; D008797:Metyrapone