Journal of Comparative Physiology B

, Volume 169, Issue 7, pp 461–573

Physiology of acute silver toxicity in the starry flounder (Platichthys stellatus) in seawater

  • C. Hogstrand
  • E. A. Ferguson
  • F. Galvez
  • J. R. Shaw
  • N. A. Webb
  • C. M. Wood
ORIGINAL PAPER

DOI: 10.1007/s003600050243

Cite this article as:
Hogstrand, C., Ferguson, E., Galvez, F. et al. J Comp Physiol B (1999) 169: 461. doi:10.1007/s003600050243
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Abstract

Physiological effects of exposure to silver (AgClnn−1; 250 μg Ag l−1 or 1000 μg Ag l−1) in seawater fish were investigated using adult starry flounders. While all fish survived up to 10 days in 250 μg Ag l−1, flounders started to die after day 4 in 1000 μg l−1. Dose-dependent increases in plasma and hepatic silver concentrations showed that silver was available for uptake. There were minimal negative effects on hematological parameters, acid-base status, and blood gases. Plasma ammonia showed a pronounced (three- to four-fold), but transient increase in flounders exposed to either 250 μg Ag l−1 or 1000 μg Ag l−1. Whole body ammonia and acid equivalent efflux measurements indicated that ammonia retention was due to a combination of stimulated production and inhibited excretion. In the 1000-μg Ag l−1 group there was a similar transient increase in plasma [magnesium], which was restored by day 4. In contrast, plasma chloride and sodium levels increased gradually towards the point when fish began to die. At 250 μg Ag l−1, the Na+/K+-ATPase activity of the intestine was unaffected but there was a two-fold increase in branchial Na+/K+-ATPase activity. The latter effect was interpreted as compensation for an elevated chloride and sodium load. The increases in plasma chloride and sodium concentrations were accompanied by a marked suppression of drinking, thereby indicating that acute silver toxicity was likely caused by a combination of elevated electrolyte concentrations and dehydration.

Key words AgOsmoregulationIonoregulationMarineFish

Copyright information

© Springer-Verlag Berlin Heidelberg 1999

Authors and Affiliations

  • C. Hogstrand
    • 1
  • E. A. Ferguson
    • 1
  • F. Galvez
    • 3
  • J. R. Shaw
    • 2
  • N. A. Webb
    • 3
  • C. M. Wood
    • 3
  1. 1.T. H. Morgan School of Biological Sciences, 101 Morgan Building, University of Kentucky, Lexington, KY 40506-0225, USA e-mail: hogstra@pop.uky.edu Tel.: +1-606-257-7751; Fax: +1-606-257-1717US
  2. 2.Graduate Center for Toxicology, 306 Health Sciences Building, University of Kentucky, Lexington, KY 40536-0305, USAUS
  3. 3.Department of Biology, 1280 Main Street W, McMaster University, Hamilton, ON L8S 4K1, CanadaCA