Costs of chronic waterborne zinc exposure and the consequences of zinc acclimation on the gill/zinc interactions of rainbow trout in hard and soft water

Derek H. Alsop, James C. McGeer, D. Gordon McDonald, Chris M. Wood

Research output: Contribution to journalArticle

86 Citations (Scopus)

Abstract

Juvenile rainbow trout were exposed to zinc in both moderately hard water (hardness = 120 mg CaCO3/L, pH = 8.0, Zn = 150 μg/L or 450 μg/L) and soft water (hardness = 20 mg CaCO3/L, pH = 7.2, Zn = 50 μg/L or 120 μg/L) for 30 d. Only the 450 μg/L zinc-exposed fish experienced significant mortality (24% in the first 2 d). Zinc exposure caused no effect on growth rate, but growth affected tissue zinc levels. Whole body zinc levels were elevated, but gills and liver showed no consistent increases relative to controls over the 30 d. Therefore, tissue zinc residues were not a good indicator of chronic zinc exposure. After the 30-d exposure, physiological function tests were performed. Zinc was 5.4 times more toxic in soft water (control 96 h LC50s in hard and soft water were 869 μg/L and 162 μg/L, respectively). All zinc-exposed trout had acclimated to the metal, as seen by an increase in the LC50 of 2.2 to 3.9 times over that seen in control fish. Physiological costs related to acclimation appeared to be few. Zinc exposure had no effect on whole body Ca2+ or Na+ levels, on resting or routine metabolic rates, or on fixed velocity sprint performance. However, critical swimming speed (U(Crit)) was significantly reduced in zinc-exposed fish, an effect that persisted in zinc-free water. Using radioisotopic techniques to distinguish new zinc incorporation, the gills were found to possess two zinc pools: a fast turnover pool (T(1/2) = 3-4 h) and a slow turnover pool (T(1/2) = days to months). The fast pool was much larger in soft water than in hard water, but at most it accounted for <3.5% of the zinc content of the gills. The size of the slow pool was unknown, but its loading rate was faster in soft water. Chronic zinc exposure was found to increase the size of the fast pool and to increase the loading rate of the slow pool.

Original languageEnglish
Pages (from-to)1014-1025
Number of pages12
JournalEnvironmental Toxicology and Chemistry
Volume18
Issue number5
StatePublished - Apr 28 1999

Fingerprint

Oncorhynchus mykiss
Acclimatization
acclimation
rainbow
Zinc
zinc
Costs and Cost Analysis
Water
cost
Costs
water
Water hardness
Fish
Fishes
exposure
Hardness
turnover
fish
Tissue
Trout

Keywords

  • Acclimation
  • Acute/chronic toxicity
  • Gill metal- binding model
  • Rainbow trout
  • Zinc

ASJC Scopus subject areas

  • Environmental Science(all)
  • Environmental Chemistry
  • Toxicology
  • Health, Toxicology and Mutagenesis

Cite this

Costs of chronic waterborne zinc exposure and the consequences of zinc acclimation on the gill/zinc interactions of rainbow trout in hard and soft water. / Alsop, Derek H.; McGeer, James C.; McDonald, D. Gordon; Wood, Chris M.

In: Environmental Toxicology and Chemistry, Vol. 18, No. 5, 28.04.1999, p. 1014-1025.

Research output: Contribution to journalArticle

@article{be2dc99c924742acab094c034213923f,
title = "Costs of chronic waterborne zinc exposure and the consequences of zinc acclimation on the gill/zinc interactions of rainbow trout in hard and soft water",
abstract = "Juvenile rainbow trout were exposed to zinc in both moderately hard water (hardness = 120 mg CaCO3/L, pH = 8.0, Zn = 150 μg/L or 450 μg/L) and soft water (hardness = 20 mg CaCO3/L, pH = 7.2, Zn = 50 μg/L or 120 μg/L) for 30 d. Only the 450 μg/L zinc-exposed fish experienced significant mortality (24{\%} in the first 2 d). Zinc exposure caused no effect on growth rate, but growth affected tissue zinc levels. Whole body zinc levels were elevated, but gills and liver showed no consistent increases relative to controls over the 30 d. Therefore, tissue zinc residues were not a good indicator of chronic zinc exposure. After the 30-d exposure, physiological function tests were performed. Zinc was 5.4 times more toxic in soft water (control 96 h LC50s in hard and soft water were 869 μg/L and 162 μg/L, respectively). All zinc-exposed trout had acclimated to the metal, as seen by an increase in the LC50 of 2.2 to 3.9 times over that seen in control fish. Physiological costs related to acclimation appeared to be few. Zinc exposure had no effect on whole body Ca2+ or Na+ levels, on resting or routine metabolic rates, or on fixed velocity sprint performance. However, critical swimming speed (U(Crit)) was significantly reduced in zinc-exposed fish, an effect that persisted in zinc-free water. Using radioisotopic techniques to distinguish new zinc incorporation, the gills were found to possess two zinc pools: a fast turnover pool (T(1/2) = 3-4 h) and a slow turnover pool (T(1/2) = days to months). The fast pool was much larger in soft water than in hard water, but at most it accounted for <3.5{\%} of the zinc content of the gills. The size of the slow pool was unknown, but its loading rate was faster in soft water. Chronic zinc exposure was found to increase the size of the fast pool and to increase the loading rate of the slow pool.",
keywords = "Acclimation, Acute/chronic toxicity, Gill metal- binding model, Rainbow trout, Zinc",
author = "Alsop, {Derek H.} and McGeer, {James C.} and McDonald, {D. Gordon} and Wood, {Chris M.}",
year = "1999",
month = "4",
day = "28",
language = "English",
volume = "18",
pages = "1014--1025",
journal = "Environmental Toxicology and Chemistry",
issn = "0730-7268",
publisher = "John Wiley and Sons Ltd",
number = "5",

}

TY - JOUR

T1 - Costs of chronic waterborne zinc exposure and the consequences of zinc acclimation on the gill/zinc interactions of rainbow trout in hard and soft water

AU - Alsop, Derek H.

AU - McGeer, James C.

AU - McDonald, D. Gordon

AU - Wood, Chris M.

PY - 1999/4/28

Y1 - 1999/4/28

N2 - Juvenile rainbow trout were exposed to zinc in both moderately hard water (hardness = 120 mg CaCO3/L, pH = 8.0, Zn = 150 μg/L or 450 μg/L) and soft water (hardness = 20 mg CaCO3/L, pH = 7.2, Zn = 50 μg/L or 120 μg/L) for 30 d. Only the 450 μg/L zinc-exposed fish experienced significant mortality (24% in the first 2 d). Zinc exposure caused no effect on growth rate, but growth affected tissue zinc levels. Whole body zinc levels were elevated, but gills and liver showed no consistent increases relative to controls over the 30 d. Therefore, tissue zinc residues were not a good indicator of chronic zinc exposure. After the 30-d exposure, physiological function tests were performed. Zinc was 5.4 times more toxic in soft water (control 96 h LC50s in hard and soft water were 869 μg/L and 162 μg/L, respectively). All zinc-exposed trout had acclimated to the metal, as seen by an increase in the LC50 of 2.2 to 3.9 times over that seen in control fish. Physiological costs related to acclimation appeared to be few. Zinc exposure had no effect on whole body Ca2+ or Na+ levels, on resting or routine metabolic rates, or on fixed velocity sprint performance. However, critical swimming speed (U(Crit)) was significantly reduced in zinc-exposed fish, an effect that persisted in zinc-free water. Using radioisotopic techniques to distinguish new zinc incorporation, the gills were found to possess two zinc pools: a fast turnover pool (T(1/2) = 3-4 h) and a slow turnover pool (T(1/2) = days to months). The fast pool was much larger in soft water than in hard water, but at most it accounted for <3.5% of the zinc content of the gills. The size of the slow pool was unknown, but its loading rate was faster in soft water. Chronic zinc exposure was found to increase the size of the fast pool and to increase the loading rate of the slow pool.

AB - Juvenile rainbow trout were exposed to zinc in both moderately hard water (hardness = 120 mg CaCO3/L, pH = 8.0, Zn = 150 μg/L or 450 μg/L) and soft water (hardness = 20 mg CaCO3/L, pH = 7.2, Zn = 50 μg/L or 120 μg/L) for 30 d. Only the 450 μg/L zinc-exposed fish experienced significant mortality (24% in the first 2 d). Zinc exposure caused no effect on growth rate, but growth affected tissue zinc levels. Whole body zinc levels were elevated, but gills and liver showed no consistent increases relative to controls over the 30 d. Therefore, tissue zinc residues were not a good indicator of chronic zinc exposure. After the 30-d exposure, physiological function tests were performed. Zinc was 5.4 times more toxic in soft water (control 96 h LC50s in hard and soft water were 869 μg/L and 162 μg/L, respectively). All zinc-exposed trout had acclimated to the metal, as seen by an increase in the LC50 of 2.2 to 3.9 times over that seen in control fish. Physiological costs related to acclimation appeared to be few. Zinc exposure had no effect on whole body Ca2+ or Na+ levels, on resting or routine metabolic rates, or on fixed velocity sprint performance. However, critical swimming speed (U(Crit)) was significantly reduced in zinc-exposed fish, an effect that persisted in zinc-free water. Using radioisotopic techniques to distinguish new zinc incorporation, the gills were found to possess two zinc pools: a fast turnover pool (T(1/2) = 3-4 h) and a slow turnover pool (T(1/2) = days to months). The fast pool was much larger in soft water than in hard water, but at most it accounted for <3.5% of the zinc content of the gills. The size of the slow pool was unknown, but its loading rate was faster in soft water. Chronic zinc exposure was found to increase the size of the fast pool and to increase the loading rate of the slow pool.

KW - Acclimation

KW - Acute/chronic toxicity

KW - Gill metal- binding model

KW - Rainbow trout

KW - Zinc

UR - http://www.scopus.com/inward/record.url?scp=0032972667&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0032972667&partnerID=8YFLogxK

M3 - Article

AN - SCOPUS:0032972667

VL - 18

SP - 1014

EP - 1025

JO - Environmental Toxicology and Chemistry

JF - Environmental Toxicology and Chemistry

SN - 0730-7268

IS - 5

ER -