Tissue-specific cadmium accumulation, metallothionein induction, and tissue zinc and copper levels during chronic sublethal cadmium exposure in juvenile rainbow trout

L. Hollis, C. Hogstrand, C. M. Wood

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Abstract

Juvenile rainbow trout, on 3% of body weight daily ration, were exposed to 0 (control) or 3 μg/L Cd (as Cd(NO3)2·4H2O) in moderately hard (140 mg/L as CaCO3), alkaline (95 mg/L as CaCO3, pH 8.0) water for 30 days. Particular attention focused on Cd burden in tissues (gills, liver, kidney, and whole body) and induction of metallothionein (MT) in gills, liver, and kidney during chronic Cd exposure. Mortality in Cd-exposed fish was minimal (∼10%), and no growth effects occurred over the 30-day exposure. Cd accumulated in a time-dependent fashion to 9 times (gills), 3 times (liver), 20 times (kidney), 2 times (carcass), and 2 times (whole body) control levels by 30 days; absolute concentrations were in the order kidney > gill > liver > whole body > carcass. Tissue (gills, liver, and kidney) Zn and Cu burdens were not altered by chronic exposure to 3 μg/L Cd. MT concentrations in all tissues increased over the 30 days of Cd exposure, but the increases were much less than those of Cd on a molar binding site basis. Absolute MT concentrations were in the order liver β kidney β gill, but relative increases were greatest in kidney (fourfold), followed by gills (twofold) and liver (1.3-fold). MT levels were sufficient to bind all Cd in gill, liver, and kidney under control conditions, and after chronic Cd exposure remained sufficient in liver and kidney, but not in gills. Total metal levels (Cd + Zn + Cu) greatly exceeded MT binding capacity in all tissues under all conditions.

Original languageEnglish
Pages (from-to)468-474
Number of pages7
JournalArchives of Environmental Contamination and Toxicology
Volume41
Issue number4
DOIs
StatePublished - Nov 12 2001

Fingerprint

metallothionein
Metallothionein
Oncorhynchus mykiss
Cadmium
Liver
rainbow
Zinc
Copper
cadmium
zinc
Tissue
copper
Kidney
cadmium-binding protein
exposure
tissue
fold
mortality
Level control
Binding sites

ASJC Scopus subject areas

  • Environmental Science(all)
  • Environmental Chemistry
  • Toxicology

Cite this

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title = "Tissue-specific cadmium accumulation, metallothionein induction, and tissue zinc and copper levels during chronic sublethal cadmium exposure in juvenile rainbow trout",
abstract = "Juvenile rainbow trout, on 3{\%} of body weight daily ration, were exposed to 0 (control) or 3 μg/L Cd (as Cd(NO3)2·4H2O) in moderately hard (140 mg/L as CaCO3), alkaline (95 mg/L as CaCO3, pH 8.0) water for 30 days. Particular attention focused on Cd burden in tissues (gills, liver, kidney, and whole body) and induction of metallothionein (MT) in gills, liver, and kidney during chronic Cd exposure. Mortality in Cd-exposed fish was minimal (∼10{\%}), and no growth effects occurred over the 30-day exposure. Cd accumulated in a time-dependent fashion to 9 times (gills), 3 times (liver), 20 times (kidney), 2 times (carcass), and 2 times (whole body) control levels by 30 days; absolute concentrations were in the order kidney > gill > liver > whole body > carcass. Tissue (gills, liver, and kidney) Zn and Cu burdens were not altered by chronic exposure to 3 μg/L Cd. MT concentrations in all tissues increased over the 30 days of Cd exposure, but the increases were much less than those of Cd on a molar binding site basis. Absolute MT concentrations were in the order liver β kidney β gill, but relative increases were greatest in kidney (fourfold), followed by gills (twofold) and liver (1.3-fold). MT levels were sufficient to bind all Cd in gill, liver, and kidney under control conditions, and after chronic Cd exposure remained sufficient in liver and kidney, but not in gills. Total metal levels (Cd + Zn + Cu) greatly exceeded MT binding capacity in all tissues under all conditions.",
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T1 - Tissue-specific cadmium accumulation, metallothionein induction, and tissue zinc and copper levels during chronic sublethal cadmium exposure in juvenile rainbow trout

AU - Hollis, L.

AU - Hogstrand, C.

AU - Wood, C. M.

PY - 2001/11/12

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N2 - Juvenile rainbow trout, on 3% of body weight daily ration, were exposed to 0 (control) or 3 μg/L Cd (as Cd(NO3)2·4H2O) in moderately hard (140 mg/L as CaCO3), alkaline (95 mg/L as CaCO3, pH 8.0) water for 30 days. Particular attention focused on Cd burden in tissues (gills, liver, kidney, and whole body) and induction of metallothionein (MT) in gills, liver, and kidney during chronic Cd exposure. Mortality in Cd-exposed fish was minimal (∼10%), and no growth effects occurred over the 30-day exposure. Cd accumulated in a time-dependent fashion to 9 times (gills), 3 times (liver), 20 times (kidney), 2 times (carcass), and 2 times (whole body) control levels by 30 days; absolute concentrations were in the order kidney > gill > liver > whole body > carcass. Tissue (gills, liver, and kidney) Zn and Cu burdens were not altered by chronic exposure to 3 μg/L Cd. MT concentrations in all tissues increased over the 30 days of Cd exposure, but the increases were much less than those of Cd on a molar binding site basis. Absolute MT concentrations were in the order liver β kidney β gill, but relative increases were greatest in kidney (fourfold), followed by gills (twofold) and liver (1.3-fold). MT levels were sufficient to bind all Cd in gill, liver, and kidney under control conditions, and after chronic Cd exposure remained sufficient in liver and kidney, but not in gills. Total metal levels (Cd + Zn + Cu) greatly exceeded MT binding capacity in all tissues under all conditions.

AB - Juvenile rainbow trout, on 3% of body weight daily ration, were exposed to 0 (control) or 3 μg/L Cd (as Cd(NO3)2·4H2O) in moderately hard (140 mg/L as CaCO3), alkaline (95 mg/L as CaCO3, pH 8.0) water for 30 days. Particular attention focused on Cd burden in tissues (gills, liver, kidney, and whole body) and induction of metallothionein (MT) in gills, liver, and kidney during chronic Cd exposure. Mortality in Cd-exposed fish was minimal (∼10%), and no growth effects occurred over the 30-day exposure. Cd accumulated in a time-dependent fashion to 9 times (gills), 3 times (liver), 20 times (kidney), 2 times (carcass), and 2 times (whole body) control levels by 30 days; absolute concentrations were in the order kidney > gill > liver > whole body > carcass. Tissue (gills, liver, and kidney) Zn and Cu burdens were not altered by chronic exposure to 3 μg/L Cd. MT concentrations in all tissues increased over the 30 days of Cd exposure, but the increases were much less than those of Cd on a molar binding site basis. Absolute MT concentrations were in the order liver β kidney β gill, but relative increases were greatest in kidney (fourfold), followed by gills (twofold) and liver (1.3-fold). MT levels were sufficient to bind all Cd in gill, liver, and kidney under control conditions, and after chronic Cd exposure remained sufficient in liver and kidney, but not in gills. Total metal levels (Cd + Zn + Cu) greatly exceeded MT binding capacity in all tissues under all conditions.

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