Abstract
A time course analysis using 110mAg, 24Na +, and 36Cl- examined gill silver accumulation and the mechanism by which waterborne silver (4.0 × 10-8 M; 4.3 μg/l) inhibits Na+ and Cl- uptake in gills of freshwater rainbow trout. Analyses of gill and body fluxes allowed calculation of apical uptake and basolateral export rates for silver, Na+, and Cl-. To avoid changes in silver bioavailability, flow-through conditions were used to limit the buildup of organic matter in the exposure water. For both Na+ and Cl- uptake, apical entry, rather than basolateral export, was the rate-limiting step; Na+ and Cl - uptake declined simultaneously and equally initially, with both uptakes reduced by ∼500 nmol·g-1·h-1 over the 1st h of silver exposure. There was a further progressive decline in Na+ uptake until 24 h. Carbonic anhydrase activity was inhibited by 1 h, whereas Na+-K+-ATPase activity was not significantly inhibited until 24 h of exposure. These results indicate that carbonic anhydrase inhibition can explain the early decline in Na+ and Cl- uptake, whereas the later decline is probably related to Na+-K +-ATPase blockade. Contrary to previous reports, gill silver accumulation increased steadily to a plateau. Despite the rapid inhibition of apical Na+ and Cl- uptake, apical silver uptake (and basolateral export) increased until 10 h, before decreasing thereafter. Thus silver did not inhibit its own apical uptake in the short term. These results suggest that reduced silver bioavailability is the mechanism behind the pattern of peak and decline in gill silver accumulation previously reported for static exposures to silver.
| Original language | English |
|---|---|
| Journal | American Journal of Physiology - Regulatory Integrative and Comparative Physiology |
| Volume | 287 |
| Issue number | 1 56-1 |
| DOIs | |
| State | Published - Jul 1 2004 |
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Keywords
- Carbonic anhydrase
- Hydrogen-adenosinetriphosphatase
- Silver uptake
- Sodium channel
- Sodium-potassium-adenosinetriphosphatase
ASJC Scopus subject areas
- Physiology
Cite this
Time course analysis of the mechanism by which silver inhibits active Na+ and Cl- uptake in gills of rainbow trout. / Morgan, Tammie P.; Grosell, Martin; Gilmour, Kathleen M.; Playle, Richard C.; Wood, Chris M.
In: American Journal of Physiology - Regulatory Integrative and Comparative Physiology, Vol. 287, No. 1 56-1, 01.07.2004.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Time course analysis of the mechanism by which silver inhibits active Na+ and Cl- uptake in gills of rainbow trout
AU - Morgan, Tammie P.
AU - Grosell, Martin
AU - Gilmour, Kathleen M.
AU - Playle, Richard C.
AU - Wood, Chris M.
PY - 2004/7/1
Y1 - 2004/7/1
N2 - A time course analysis using 110mAg, 24Na +, and 36Cl- examined gill silver accumulation and the mechanism by which waterborne silver (4.0 × 10-8 M; 4.3 μg/l) inhibits Na+ and Cl- uptake in gills of freshwater rainbow trout. Analyses of gill and body fluxes allowed calculation of apical uptake and basolateral export rates for silver, Na+, and Cl-. To avoid changes in silver bioavailability, flow-through conditions were used to limit the buildup of organic matter in the exposure water. For both Na+ and Cl- uptake, apical entry, rather than basolateral export, was the rate-limiting step; Na+ and Cl - uptake declined simultaneously and equally initially, with both uptakes reduced by ∼500 nmol·g-1·h-1 over the 1st h of silver exposure. There was a further progressive decline in Na+ uptake until 24 h. Carbonic anhydrase activity was inhibited by 1 h, whereas Na+-K+-ATPase activity was not significantly inhibited until 24 h of exposure. These results indicate that carbonic anhydrase inhibition can explain the early decline in Na+ and Cl- uptake, whereas the later decline is probably related to Na+-K +-ATPase blockade. Contrary to previous reports, gill silver accumulation increased steadily to a plateau. Despite the rapid inhibition of apical Na+ and Cl- uptake, apical silver uptake (and basolateral export) increased until 10 h, before decreasing thereafter. Thus silver did not inhibit its own apical uptake in the short term. These results suggest that reduced silver bioavailability is the mechanism behind the pattern of peak and decline in gill silver accumulation previously reported for static exposures to silver.
AB - A time course analysis using 110mAg, 24Na +, and 36Cl- examined gill silver accumulation and the mechanism by which waterborne silver (4.0 × 10-8 M; 4.3 μg/l) inhibits Na+ and Cl- uptake in gills of freshwater rainbow trout. Analyses of gill and body fluxes allowed calculation of apical uptake and basolateral export rates for silver, Na+, and Cl-. To avoid changes in silver bioavailability, flow-through conditions were used to limit the buildup of organic matter in the exposure water. For both Na+ and Cl- uptake, apical entry, rather than basolateral export, was the rate-limiting step; Na+ and Cl - uptake declined simultaneously and equally initially, with both uptakes reduced by ∼500 nmol·g-1·h-1 over the 1st h of silver exposure. There was a further progressive decline in Na+ uptake until 24 h. Carbonic anhydrase activity was inhibited by 1 h, whereas Na+-K+-ATPase activity was not significantly inhibited until 24 h of exposure. These results indicate that carbonic anhydrase inhibition can explain the early decline in Na+ and Cl- uptake, whereas the later decline is probably related to Na+-K +-ATPase blockade. Contrary to previous reports, gill silver accumulation increased steadily to a plateau. Despite the rapid inhibition of apical Na+ and Cl- uptake, apical silver uptake (and basolateral export) increased until 10 h, before decreasing thereafter. Thus silver did not inhibit its own apical uptake in the short term. These results suggest that reduced silver bioavailability is the mechanism behind the pattern of peak and decline in gill silver accumulation previously reported for static exposures to silver.
KW - Carbonic anhydrase
KW - Hydrogen-adenosinetriphosphatase
KW - Silver uptake
KW - Sodium channel
KW - Sodium-potassium-adenosinetriphosphatase
UR - http://www.scopus.com/inward/record.url?scp=3042810405&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=3042810405&partnerID=8YFLogxK
U2 - 10.1152/ajpregu.00448.2003
DO - 10.1152/ajpregu.00448.2003
M3 - Article
C2 - 15016622
AN - SCOPUS:3042810405
VL - 287
JO - American Journal of Physiology - Cell Physiology
JF - American Journal of Physiology - Cell Physiology
SN - 0363-6143
IS - 1 56-1
ER -