title: Acute exposure to waterborne copper inhibits both the excretion and uptake of ammonia in freshwater rainbow trout (Oncorhynchus mykiss).
abstract: In freshwater fish, exposure to sub-lethal concentrations of waterborne copper (Cu) results in inhibitions of ammonia excretion (Jamm) and Na(+) uptake (J(Na)in), yet the mechanisms by which these occur are not fully understood. In the present study, rainbow trout (Oncorhynchus mykiss) fry exposed to 50μg/l Cu for 24h displayed a sustained 40% decrease in Jamm and a transient 60% decrease in J(Na)in. Previously, these effects have been attributed to inhibitions of gill Na(+)/K(+)-ATPase and/or carbonic anhydrase (CA) activities by Cu. Trout fry did not display significant reductions in the branchial activities of these enzymes or H(+)-ATPase over 24h Cu exposure. Recently, Rhesus (Rh) glycoproteins, bi-directional NH3 gas channels, have been implicated in the mechanism of Cu toxicity. Juvenile trout were exposed to nominal 0, 50, and 200μg/l Cu for 3-6h under control conditions (ammonia-free water) followed by 6h exposure to high environmental ammonia (HEA; 1.5mmol/l NH4HCO3). HEA led to significant ammonia uptake in control fish (0μg/l Cu), and exposure to 50 and 200μg/l Cu resulted in significant reductions of ammonia uptake during HEA exposure. This is the first evidence that Cu inhibits both the excretion and uptake of ammonia, implicating bi-directional Rh glycoproteins as a target for Cu toxicity. We propose a model whereby Rh blockade by Cu causes the sustained inhibition of Jamm and transient inhibition of J(Na)in, with H(+)-ATPase potentially aiding in J(Na)in recovery. More work is needed to elucidate the role of Rh proteins in sub-lethal Cu toxicity.
authors.affiliation: Department of Biology, McMaster University, Hamilton L8S 4K1, ON, Canada. Electronic address: limmy@mcmaster.ca.
authors.forename: Michael Yu-Ting
authors.initials: MY
authors.lastname: Lim
authors.affiliation: Department of Biology, McMaster University, Hamilton L8S 4K1, ON, Canada. Electronic address: zimmea@mcmaster.ca.
authors.forename: Alex M
authors.initials: AM
authors.lastname: Zimmer
authors.affiliation: Department of Biology, McMaster University, Hamilton L8S 4K1, ON, Canada; Department of Zoology, University of British Columbia, Vancouver V6T 1Z4, BC, Canada. Electronic address: woodcm@mcmaster.ca.
authors.forename: Chris M
authors.initials: CM
authors.lastname: Wood
mesh_terms: D000641:Ammonia / Q000378:metabolism*; D000818:Animals; D001692:Biological Transport / Q000187:drug effects*; D003300:Copper / Q000009:adverse effects*; D004781:Environmental Exposure / Q000009:adverse effects*; D029941:Fish Proteins / Q000378:metabolism; D005618:Fresh Water; D017686:Oncorhynchus mykiss / Q000378:metabolism / Q000502:physiology*; D006180:Proton-Translocating ATPases / Q000378:metabolism; D012964:Sodium / Q000378:metabolism; D000254:Sodium-Potassium-Exchanging ATPase / Q000378:metabolism; D014874:Water Pollutants, Chemical / Q000009:adverse effects
chemical_list: D029941:Fish Proteins; D014874:Water Pollutants, Chemical; D000641:Ammonia; D003300:Copper; D012964:Sodium; D006180:Proton-Translocating ATPases; D000254:Sodium-Potassium-Exchanging ATPase
keywords: Ammonia excretion (J(amm)); Carbonic anhydrase (CA); Copper; H(+)-ATPase; High environmental ammonia (HEA); Na(+)/K(+)-ATPase; Rhesus (Rh) glycoproteins; Sodium uptake (J(Na)(in))