Dietary sodium inhibits aqueous copper uptake in rainbow trout (Oncorhynchus mykiss)
G. G. Pyle1,2,*,
C. N. Kamunde2,
D. G. McDonald2,3 and
C. M. Wood2
1 Dept of Biology, Nipissing University, North Bay, Ontario, P1B 8L7,
Canada
2 Dept of Biology, McMaster University, Hamilton, Ontario, L8S 4K1,
Canada
3 Dept of Zoology, University of Guelph, Guelph, Ontario, N1G 2W1,
Canada
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Fig. 1. New copper uptake rate (as defined by equation 1) into rainbow trout fed
for 7 days on diets ranging in sodium concentration after a subsequent 6 h
exposure to 20 µg l-1 of waterborne copper. Bars represent means
± S.E.M., N=4-5. Asterisks represent significant difference
from control (0.6%) diet (P<0.05).
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Fig. 2. Newly accumulated copper (as defined by equation 1) in gills, liver,
kidney, blood plasma and gut (inset) of rainbow trout fed for 7 days on diets
ranging in sodium concentration after a subsequent 6 h exposure to 20 µg
l-1 of waterborne copper. Points represent means ± S.E.M.,
N=4-5. Asterisks represent significant difference from control (0.6%)
diet (P<0.05).
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Fig. 3. Total copper concentrations in gills (A) and livers (B) of rainbow trout
fed for 7 days on diets ranging in sodium concentration after a subsequent 6 h
exposure to 20 µg l-1 of waterborne copper. Points represent
means ± S.E.M., N=4-5. Asterisks represent significant
difference from control (0.6%) diet (P<0.05).
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Fig. 4. Total sodium concentrations in gut tissue and plasma of rainbow trout fed
for 7 days on diets ranging in sodium concentration after a subsequent 6 h
exposure to 20 µg l-1 of waterborne copper. Points represent
means ± S.E.M., N=4-5. Asterisks represent significant
difference from control (0.6%) diet (P<0.05).
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Fig. 5. Sodium influx, efflux and net flux rates into juvenile rainbow trout fed
for 7 days on diets ranging in sodium concentration after a subsequent 6 h
exposure to 20 µg l-1 of waterborne copper. Sodium influx rates
were determined on individual fish, which facilitated the calculation of means
and S.E.M. (bars; N=4-5) and statistical comparisons (asterisks
indicate statistical significance at P<0.05). However, efflux
rates were determined on groups of fish that precluded statistical comparisons
among treatment groups for efflux or net flux data.
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Fig. 6. Branchial Na+/K+-ATPase activity in rainbow trout
exposed to different feeding regimes and waterborne copper concentrations.
Experimental treatments included feeding fish 3% of their total body mass per
day on untreated food (`Fed') or feeding fish 3% of their total body mass per
day on food that was supplemented with 3% sodium by mass (`Na Fed'). Fish were
then exposed to either no copper in the water or to 20 µg l-1 of
dissolved copper (Cu) for 6 h. Bars represent means ± S.E.M.,
N=5-6, bars sharing the same letter are not significantly different
from one another (P>0.05).
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Fig. 7. New sodium (A) and copper (B) accumulation (as defined by equation 1) in
gills of rainbow trout exposed to a normal diet and no waterborne Cu (`Fed'),
a normal diet and 20 µg l-1 waterborne Cu (`Fed+Cu') or a diet
supplemented with 3% Na+ by mass and 20 µg l-1
waterborne Cu (`Na Fed+Cu'). Bars represent means ± S.E.M.,
N=5-6, bars sharing the same letter are not significantly different
from one another (P>0.05).
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Fig. 8. Drinking rates in rainbow trout that were either starved (`Unfed'), fed 3%
of their total mass on a normal diet (`Fed') or fed 3% of their total mass on
a diet supplemented with 3% Na+ by mass (`Na Fed') for 7 days. Bars
represent means ± S.E.M., N=5. Bars sharing the same letter
are not significantly different from one another (P>0.05).
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Fig. 9. Conceptual model of sodium and copper regulation in chloride cells of
rainbow trout gills, including a common apical channel shared between sodium
and copper (broken line). As sodium absorbed from the diet accumulates in
these cells, the apical channel is downregulated. This results in reduced
sodium and copper uptake, which is thought to be the mechanism by which
dietary sodium protects against waterborne copper exposure. Details are given
in the text.
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© The Company of Biologists Ltd 2003
