Abstract
Gulf toadfish were exposed to sublethal levels of copper (12.8 or 55.2 μM) for 30 days. Drinking in control fish averaged 1 ml kg-1 h-1 but exposure to 55.2 μM copper resulted in a complex biophasic pattern with initial (3 h and 1 day) inhibition of drinking rate, followed by an elevation of drinking rate from day 3 onwards. Drinking led to copper accumulation in the intestinal fluids at levels three to five times higher than the ambient copper concentrations, which in turn resulted in intestinal copper accumulation. The gill exhibited more rapid accumulation of copper than the intestine and contributed to early copper uptake leading to accumulation in internal organs. Muscle, spleen and plasma exhibited little if any disturbance of copper homeostasis while renal copper accumulation was evident at both ambient copper concentrations. The liver exhibited the highest copper concentrations and the greatest copper accumulation of all examined internal organs during exposure to 55.2 μM. Elevated biliary copper excretion was evident from measurements of gall bladder bile copper concentrations and appeared to protect partially against internal accumulation in fish exposed to 12.8 μM copper. No inhibition of Na+/K+-ATPase activity in either gills or intestine was seen despite copper accumulation in these organs. Calculations of inorganic copper speciation suggest that Cu(CO 3)22- complexes which dominate in seawater and intestinal fluids are of limited availability for uptake while the low levels of ionic Cu2+, CuOH+ and CuCO3 may be the forms taken up by the gill and the intestinal epithelium.
| Original language | English |
|---|---|
| Pages (from-to) | 263-275 |
| Number of pages | 13 |
| Journal | Aquatic Toxicology |
| Volume | 68 |
| Issue number | 3 |
| DOIs | |
| State | Published - Jun 24 2004 |
Fingerprint
Keywords
- Cu homeostasis
- Cu speciation
- Cu uptake
- Hepatobiliary excretion
- Intestinal fluid Cu
ASJC Scopus subject areas
- Aquatic Science
Cite this
Effects of prolonged copper exposure in the marine gulf toadfish (Opsanus beta) II : Copper accumulation, drinking rate and Na+/K +-ATPase activity in osmoregulatory tissues. / Grosell, Martin; Mcdonald, Danielle M; Walsh, P. J.; Wood, C. M.
In: Aquatic Toxicology, Vol. 68, No. 3, 24.06.2004, p. 263-275.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Effects of prolonged copper exposure in the marine gulf toadfish (Opsanus beta) II
T2 - Copper accumulation, drinking rate and Na+/K +-ATPase activity in osmoregulatory tissues
AU - Grosell, Martin
AU - Mcdonald, Danielle M
AU - Walsh, P. J.
AU - Wood, C. M.
PY - 2004/6/24
Y1 - 2004/6/24
N2 - Gulf toadfish were exposed to sublethal levels of copper (12.8 or 55.2 μM) for 30 days. Drinking in control fish averaged 1 ml kg-1 h-1 but exposure to 55.2 μM copper resulted in a complex biophasic pattern with initial (3 h and 1 day) inhibition of drinking rate, followed by an elevation of drinking rate from day 3 onwards. Drinking led to copper accumulation in the intestinal fluids at levels three to five times higher than the ambient copper concentrations, which in turn resulted in intestinal copper accumulation. The gill exhibited more rapid accumulation of copper than the intestine and contributed to early copper uptake leading to accumulation in internal organs. Muscle, spleen and plasma exhibited little if any disturbance of copper homeostasis while renal copper accumulation was evident at both ambient copper concentrations. The liver exhibited the highest copper concentrations and the greatest copper accumulation of all examined internal organs during exposure to 55.2 μM. Elevated biliary copper excretion was evident from measurements of gall bladder bile copper concentrations and appeared to protect partially against internal accumulation in fish exposed to 12.8 μM copper. No inhibition of Na+/K+-ATPase activity in either gills or intestine was seen despite copper accumulation in these organs. Calculations of inorganic copper speciation suggest that Cu(CO 3)22- complexes which dominate in seawater and intestinal fluids are of limited availability for uptake while the low levels of ionic Cu2+, CuOH+ and CuCO3 may be the forms taken up by the gill and the intestinal epithelium.
AB - Gulf toadfish were exposed to sublethal levels of copper (12.8 or 55.2 μM) for 30 days. Drinking in control fish averaged 1 ml kg-1 h-1 but exposure to 55.2 μM copper resulted in a complex biophasic pattern with initial (3 h and 1 day) inhibition of drinking rate, followed by an elevation of drinking rate from day 3 onwards. Drinking led to copper accumulation in the intestinal fluids at levels three to five times higher than the ambient copper concentrations, which in turn resulted in intestinal copper accumulation. The gill exhibited more rapid accumulation of copper than the intestine and contributed to early copper uptake leading to accumulation in internal organs. Muscle, spleen and plasma exhibited little if any disturbance of copper homeostasis while renal copper accumulation was evident at both ambient copper concentrations. The liver exhibited the highest copper concentrations and the greatest copper accumulation of all examined internal organs during exposure to 55.2 μM. Elevated biliary copper excretion was evident from measurements of gall bladder bile copper concentrations and appeared to protect partially against internal accumulation in fish exposed to 12.8 μM copper. No inhibition of Na+/K+-ATPase activity in either gills or intestine was seen despite copper accumulation in these organs. Calculations of inorganic copper speciation suggest that Cu(CO 3)22- complexes which dominate in seawater and intestinal fluids are of limited availability for uptake while the low levels of ionic Cu2+, CuOH+ and CuCO3 may be the forms taken up by the gill and the intestinal epithelium.
KW - Cu homeostasis
KW - Cu speciation
KW - Cu uptake
KW - Hepatobiliary excretion
KW - Intestinal fluid Cu
UR - http://www.scopus.com/inward/record.url?scp=2542498725&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=2542498725&partnerID=8YFLogxK
U2 - 10.1016/j.aquatox.2004.03.007
DO - 10.1016/j.aquatox.2004.03.007
M3 - Article
C2 - 15159052
AN - SCOPUS:2542498725
VL - 68
SP - 263
EP - 275
JO - Aquatic Toxicology
JF - Aquatic Toxicology
SN - 0166-445X
IS - 3
ER -