Waterborne copper exposure inhibits ammonia excretion and branchial carbonic anhydrase activity in euryhaline guppies acclimated to both fresh water and sea water

Inhibition of ammonia excretion (Jamm) 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 20 μg Cu/l in FW (0 ppt) and SW (25 ppt) for 96 h. In both salinities, Cu transiently inhibited ammonia excretion (Jamm) followed by a full recovery by the end of the 96 h exposure. The activities of Na+/K+-ATPase, H+-ATPase, and carbonic anhydrase (CA) were examined in the gills at 12 and 96 h of Cu exposure. In both salinity acclimations, CA activity was significantly inhibited following 12 h 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 Jamm in both salinity acclimations. The blockade of CA potentially acts as a common mechanism of Jamm 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 96 h relative to the 12 h time point, potentially involving this enzyme in re-establishing Jamm.

► First evidence of in vivo inhibition of carbonic anhydrase by waterborne Cu in fish.
► Concomitant inhibition of ammonia excretion and gill carbonic anhydrase activity.
► Both recover despite continued Cu exposure in both fresh and sea water.