Metal toxicity in fish is expected to be most severe in soft waters because of the low availability of cations (particularly Ca2+) to out-compete the metal forms for binding sites on the gills. Natural waters in the Amazon basin are typically soft due to regional geochemistry, but few studies have focused on metal toxicity in fish native to the basin. We assessed the ionoregulatory effects of waterborne copper (Cu) and cadmium (Cd) on tambaqui (Colossoma macropomum) in extremely soft water (10 μmol l -1 Ca2+). Tambaqui had a very high tolerance to Cu (50-400 μg l-1), as indicated by a complete lack of inhibition of Na + uptake and an ability to gradually recover over 6 h from elevated diffusive Na+ losses caused by Cu. The insensitivity of active Na+ influx to Cu further supports the notion that Amazonian fish may have a unique Na+ transport system. Addition of 5-10 mg C l -1 of dissolved organic matter (DOM) did not prevent initial (0-3 h) negative Na+ balance in tambaqui exposed to Cu. Exposure to 40 mg C l-1 DOM prevented Na+ losses in tambaqui even at 400 μg l-1 Cu, probably because most Cu was complexed to DOM. Tambaqui exposed to waterborne Cd (10-80 μg l-1) experienced an average of 42% inhibition in whole body Ca2+ uptake relative to controls within 3 h of exposure to the metal. Inhibition of Ca2+ uptake increased over time and, at 24 h, Ca2+ uptake was suppressed by 51% and 91% in fish exposed to 10 and 80 μg l-1 Cd, respectively. Previous acclimation of fish to either elevated [Ca2+] or elevated [DOM] proved to be very effective in protecting against acute short-term metal accumulation at the gills of tambaqui in soft water (in the absence of the protective agent during metal exposure), suggesting a conditioning effect on gill metal binding physiology. © 2005 Elsevier B.V. All rights reserved.
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