TY - JOUR
T1 - Acute exposure to waterborne copper inhibits both the excretion and uptake of ammonia in freshwater rainbow trout (Oncorhynchus mykiss)
AU - Lim, Michael Yu Ting
AU - Zimmer, Alex M.
AU - Wood, Chris M.
N1 - Funding Information:
Special thanks to Dr. Scott Smith, Wilfrid Laurier University, for helpful information regarding the chemical speciation of Cu and ammonia. Thanks also to two anonymous referees for constructive comments which improved the manuscript. This research was supported by an NSERC (Natural Sciences and Engineering Research Council of Canada) ( RGPIN473-12 ) Discovery Grant to CMW, who was also supported by the Canada Research Chairs . AMZ is supported by an NSERC Canada Graduate Scholarship.
Publisher Copyright:
© 2014 Elsevier Inc. All rights reserved.
Copyright:
Copyright 2020 Elsevier B.V., All rights reserved.
PY - 2015/2
Y1 - 2015/2
N2 - In freshwater fish, exposure to sub-lethal concentrations of waterborne copper (Cu) results in inhibitions of ammonia excretion (Jamm) and Na+ uptake (JNa
in), yet the mechanisms by which these occur are not fully understood. In the present study, rainbow trout (Oncorhynchus mykiss) fry exposed to 50 μg/l Cu for 24 h displayed a sustained 40% decrease in Jamm and a transient 60% decrease in JNa
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 24 h Cu exposure. Recently, Rhesus (Rh) glycoproteins, bi-directional NH3 gas channels, have been implicated in the mechanismof Cu toxicity. Juvenile trout were exposed to nominal 0, 50, and 200 μg/l Cu for 3-6 h under control conditions (ammonia-free water) followed by 6 h exposure to high environmental ammonia (HEA; 1.5 mmol/l NH4HCO3). HEA led to significant ammonia uptake in control fish (0 μg/l Cu), and exposure to 50 and 200 μg/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 JNa
in, with H+-ATPase potentially aiding in JNa
in recovery. More work is needed to elucidate the role of Rh proteins in sub-lethal Cu toxicity.
AB - In freshwater fish, exposure to sub-lethal concentrations of waterborne copper (Cu) results in inhibitions of ammonia excretion (Jamm) and Na+ uptake (JNa
in), yet the mechanisms by which these occur are not fully understood. In the present study, rainbow trout (Oncorhynchus mykiss) fry exposed to 50 μg/l Cu for 24 h displayed a sustained 40% decrease in Jamm and a transient 60% decrease in JNa
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 24 h Cu exposure. Recently, Rhesus (Rh) glycoproteins, bi-directional NH3 gas channels, have been implicated in the mechanismof Cu toxicity. Juvenile trout were exposed to nominal 0, 50, and 200 μg/l Cu for 3-6 h under control conditions (ammonia-free water) followed by 6 h exposure to high environmental ammonia (HEA; 1.5 mmol/l NH4HCO3). HEA led to significant ammonia uptake in control fish (0 μg/l Cu), and exposure to 50 and 200 μg/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 JNa
in, with H+-ATPase potentially aiding in JNa
in recovery. More work is needed to elucidate the role of Rh proteins in sub-lethal Cu toxicity.
KW - Ammonia excretion (J)
KW - Carbonic anhydrase (CA)
KW - Copper
KW - H-ATPase
KW - High environmental ammonia (HEA)
KW - Na/K-ATPase
KW - Rhesus (Rh) glycoproteins
KW - Sodium uptake (J )
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U2 - 10.1016/j.cbpc.2014.12.002
DO - 10.1016/j.cbpc.2014.12.002
M3 - Article
AN - SCOPUS:84919903995
VL - 168
SP - 48
EP - 54
JO - Comparative Biochemistry and Physiology Part - C: Toxicology and Pharmacology
JF - Comparative Biochemistry and Physiology Part - C: Toxicology and Pharmacology
SN - 1532-0456
ER -