TY - JOUR
T1 - Waterborne copper exposure inhibits ammonia excretion and branchial carbonic anhydrase activity in euryhaline guppies acclimated to both fresh water and sea water
AU - Zimmer, Alex M.
AU - Barcarolli, Indianara Fernanda
AU - Wood, Chris M.
AU - Bianchini, Adalto
N1 - Funding Information:
Special thanks to Drs. Elton Pinto Colares and Juliano Zanette for providing P. vivipara that were crucial to the completion of this study and to Marianna Basso Jorge for technical assistance and guidance with enzymatic assays. This research was supported by an award from the International Development Research Centre (IDRC) and the Canada Research Chair Program to AB and CMW and an award from the Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq) from Brazil to AB in the scope of the Instituto Nacional de Ciência e Tecnologia de Toxicologia Aquática (INCT-TA). This work was also supported by an NSERC CRD grant (Scott Smith, P.I) with co-funding from the International Zinc Association (IZA), the International Lead Zinc Research Organization (ILZRO), the Nickel Producers Environmental Research Association (NiPERA), the International Copper Association (ICA), the Copper Development Association (CDA), Teck Resources , and Vale Inco . CMW is supported by the Canada Research Chair Program. A. Bianchini is a research fellow from the Brazilian CNPq (Proc. #304430/2009-9), and is supported by the International Research Chair Program from IDRC .
PY - 2012/10/15
Y1 - 2012/10/15
N2 - Inhibition of ammonia excretion (J amm) is a common response to Cu exposure in freshwater (FW) and seawater (SW) organisms. To determine the mechanism of this response, a euryhaline species of guppy (Poecilia vivipara) was exposed to 20μg Cu/l in FW (0ppt) and SW (25ppt) for 96h. In both salinities, Cu transiently inhibited ammonia excretion (J amm) followed by a full recovery by the end of the 96h exposure. The activities of Na +/K +-ATPase, H +-ATPase, and carbonic anhydrase (CA) were examined in the gills at 12 and 96h of Cu exposure. In both salinity acclimations, CA activity was significantly inhibited following 12h of Cu exposure in P. vivipara, marking the first in vivo evidence of Cu-induced inhibition of CA in fish. Moreover, the inhibition and recovery of this enzyme were correlated with the inhibition and recovery of J amm in both salinity acclimations. The blockade of CA potentially acts as a common mechanism of J amm inhibition in FW and SW. There were no significant effects on Na +/K +-ATPase or H +-ATPase activity at either time point or salinity. However, H +-ATPase activity was upregulated at 96h relative to the 12h time point, potentially involving this enzyme in re-establishing J amm.
AB - Inhibition of ammonia excretion (J amm) is a common response to Cu exposure in freshwater (FW) and seawater (SW) organisms. To determine the mechanism of this response, a euryhaline species of guppy (Poecilia vivipara) was exposed to 20μg Cu/l in FW (0ppt) and SW (25ppt) for 96h. In both salinities, Cu transiently inhibited ammonia excretion (J amm) followed by a full recovery by the end of the 96h exposure. The activities of Na +/K +-ATPase, H +-ATPase, and carbonic anhydrase (CA) were examined in the gills at 12 and 96h of Cu exposure. In both salinity acclimations, CA activity was significantly inhibited following 12h of Cu exposure in P. vivipara, marking the first in vivo evidence of Cu-induced inhibition of CA in fish. Moreover, the inhibition and recovery of this enzyme were correlated with the inhibition and recovery of J amm in both salinity acclimations. The blockade of CA potentially acts as a common mechanism of J amm inhibition in FW and SW. There were no significant effects on Na +/K +-ATPase or H +-ATPase activity at either time point or salinity. However, H +-ATPase activity was upregulated at 96h relative to the 12h time point, potentially involving this enzyme in re-establishing J amm.
KW - Ammonia excretion (J )
KW - Carbonic anhydrase (CA)
KW - Copper (Cu)
KW - Euryhaline
KW - Poecilia vivipara
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U2 - 10.1016/j.aquatox.2012.06.010
DO - 10.1016/j.aquatox.2012.06.010
M3 - Article
C2 - 22819806
AN - SCOPUS:84864054648
VL - 122-123
SP - 172
EP - 180
JO - Aquatic Toxicology
JF - Aquatic Toxicology
SN - 0166-445X
ER -