Hydromineral balance in the marine gulf toadfish (Opsanus beta) exposed to waterborne or infused nickel

Eric F. Pane, Danielle M Mcdonald, H. Nathan Curry, Jonathan Blanchard, Chris M. Wood, Martin Grosell

Research output: Contribution to journalArticle

11 Citations (Scopus)

Abstract

The effects of acute Ni exposure on the marine gulf toadfish (Opsanus beta) were investigated via separate exposures to waterborne nickel (Ni) and arterially infused Ni. Of the plasma electrolytes measured after 72 h of waterborne exposure (215.3 and 606.1 μM Ni in SW (salinity of 34)), only plasma [Ca2+] was significantly impacted (∼55% decrease at both exposure concentrations). At both exposure concentrations, plasma [Ni] was regulated for 24 h, after which a linear accumulation over time occurred. Accumulation of Ni in the plasma, and in tissues in direct contact with seawater (gill, stomach, and intestine), was roughly proportional to the Ni concentration of the exposure water. Hydromineral balance in the intestinal fluid (IF) was markedly impacted, with Na+, Cl-, SO42-, K+, and Mg2+ concentrations elevated after 72 h of exposure to waterborne Ni. Following arterial Ni infusion (0.40 μmol Ni kg-1 h-1), perturbation of hydromineral balance of the intestinal fluid was specific only to Na+ (significantly elevated by Ni infusion) and Mg2+ (significantly decreased by Ni infusion). Nitrogen excretion was not significantly impacted by Ni infusion. In all tissues save the kidney, Ni accumulation via infusion was only a fraction of that observed during waterborne exposures. Remarkably, the kidney Ni burden following infusion was almost identical to that resulting from both waterborne exposures, suggesting homeostatic control. Ni excretion, dominated at 24 h by extrarenal routes, was primarily a function of renal excretion by 72 h of infusion. The sum excretion from infused toadfish was relatively efficient, accounting for over 40% of the infused dose by 72 h. Mechanistic knowledge of the mechanisms of toxicity of waterborne Ni in marine systems is a critical component to the development of physiologically based modeling approaches to accurately predict Ni toxicity in marine and estuarine ecosystems.

Original languageEnglish
Pages (from-to)70-81
Number of pages12
JournalAquatic Toxicology
Volume80
Issue number1
DOIs
StatePublished - Oct 25 2006

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Batrachoidiformes
Nickel
nickel
excretion
Opsanus beta
gulf
plasma
kidneys

Keywords

  • Excretion
  • Gulf toadfish
  • Infusion
  • Ion balance
  • Marine toxicity
  • Mechanistic physiology
  • Nickel
  • Waterborne

ASJC Scopus subject areas

  • Aquatic Science

Cite this

Hydromineral balance in the marine gulf toadfish (Opsanus beta) exposed to waterborne or infused nickel. / Pane, Eric F.; Mcdonald, Danielle M; Curry, H. Nathan; Blanchard, Jonathan; Wood, Chris M.; Grosell, Martin.

In: Aquatic Toxicology, Vol. 80, No. 1, 25.10.2006, p. 70-81.

Research output: Contribution to journalArticle

Pane, Eric F. ; Mcdonald, Danielle M ; Curry, H. Nathan ; Blanchard, Jonathan ; Wood, Chris M. ; Grosell, Martin. / Hydromineral balance in the marine gulf toadfish (Opsanus beta) exposed to waterborne or infused nickel. In: Aquatic Toxicology. 2006 ; Vol. 80, No. 1. pp. 70-81.
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abstract = "The effects of acute Ni exposure on the marine gulf toadfish (Opsanus beta) were investigated via separate exposures to waterborne nickel (Ni) and arterially infused Ni. Of the plasma electrolytes measured after 72 h of waterborne exposure (215.3 and 606.1 μM Ni in SW (salinity of 34)), only plasma [Ca2+] was significantly impacted (∼55{\%} decrease at both exposure concentrations). At both exposure concentrations, plasma [Ni] was regulated for 24 h, after which a linear accumulation over time occurred. Accumulation of Ni in the plasma, and in tissues in direct contact with seawater (gill, stomach, and intestine), was roughly proportional to the Ni concentration of the exposure water. Hydromineral balance in the intestinal fluid (IF) was markedly impacted, with Na+, Cl-, SO42-, K+, and Mg2+ concentrations elevated after 72 h of exposure to waterborne Ni. Following arterial Ni infusion (0.40 μmol Ni kg-1 h-1), perturbation of hydromineral balance of the intestinal fluid was specific only to Na+ (significantly elevated by Ni infusion) and Mg2+ (significantly decreased by Ni infusion). Nitrogen excretion was not significantly impacted by Ni infusion. In all tissues save the kidney, Ni accumulation via infusion was only a fraction of that observed during waterborne exposures. Remarkably, the kidney Ni burden following infusion was almost identical to that resulting from both waterborne exposures, suggesting homeostatic control. Ni excretion, dominated at 24 h by extrarenal routes, was primarily a function of renal excretion by 72 h of infusion. The sum excretion from infused toadfish was relatively efficient, accounting for over 40{\%} of the infused dose by 72 h. Mechanistic knowledge of the mechanisms of toxicity of waterborne Ni in marine systems is a critical component to the development of physiologically based modeling approaches to accurately predict Ni toxicity in marine and estuarine ecosystems.",
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N2 - The effects of acute Ni exposure on the marine gulf toadfish (Opsanus beta) were investigated via separate exposures to waterborne nickel (Ni) and arterially infused Ni. Of the plasma electrolytes measured after 72 h of waterborne exposure (215.3 and 606.1 μM Ni in SW (salinity of 34)), only plasma [Ca2+] was significantly impacted (∼55% decrease at both exposure concentrations). At both exposure concentrations, plasma [Ni] was regulated for 24 h, after which a linear accumulation over time occurred. Accumulation of Ni in the plasma, and in tissues in direct contact with seawater (gill, stomach, and intestine), was roughly proportional to the Ni concentration of the exposure water. Hydromineral balance in the intestinal fluid (IF) was markedly impacted, with Na+, Cl-, SO42-, K+, and Mg2+ concentrations elevated after 72 h of exposure to waterborne Ni. Following arterial Ni infusion (0.40 μmol Ni kg-1 h-1), perturbation of hydromineral balance of the intestinal fluid was specific only to Na+ (significantly elevated by Ni infusion) and Mg2+ (significantly decreased by Ni infusion). Nitrogen excretion was not significantly impacted by Ni infusion. In all tissues save the kidney, Ni accumulation via infusion was only a fraction of that observed during waterborne exposures. Remarkably, the kidney Ni burden following infusion was almost identical to that resulting from both waterborne exposures, suggesting homeostatic control. Ni excretion, dominated at 24 h by extrarenal routes, was primarily a function of renal excretion by 72 h of infusion. The sum excretion from infused toadfish was relatively efficient, accounting for over 40% of the infused dose by 72 h. Mechanistic knowledge of the mechanisms of toxicity of waterborne Ni in marine systems is a critical component to the development of physiologically based modeling approaches to accurately predict Ni toxicity in marine and estuarine ecosystems.

AB - The effects of acute Ni exposure on the marine gulf toadfish (Opsanus beta) were investigated via separate exposures to waterborne nickel (Ni) and arterially infused Ni. Of the plasma electrolytes measured after 72 h of waterborne exposure (215.3 and 606.1 μM Ni in SW (salinity of 34)), only plasma [Ca2+] was significantly impacted (∼55% decrease at both exposure concentrations). At both exposure concentrations, plasma [Ni] was regulated for 24 h, after which a linear accumulation over time occurred. Accumulation of Ni in the plasma, and in tissues in direct contact with seawater (gill, stomach, and intestine), was roughly proportional to the Ni concentration of the exposure water. Hydromineral balance in the intestinal fluid (IF) was markedly impacted, with Na+, Cl-, SO42-, K+, and Mg2+ concentrations elevated after 72 h of exposure to waterborne Ni. Following arterial Ni infusion (0.40 μmol Ni kg-1 h-1), perturbation of hydromineral balance of the intestinal fluid was specific only to Na+ (significantly elevated by Ni infusion) and Mg2+ (significantly decreased by Ni infusion). Nitrogen excretion was not significantly impacted by Ni infusion. In all tissues save the kidney, Ni accumulation via infusion was only a fraction of that observed during waterborne exposures. Remarkably, the kidney Ni burden following infusion was almost identical to that resulting from both waterborne exposures, suggesting homeostatic control. Ni excretion, dominated at 24 h by extrarenal routes, was primarily a function of renal excretion by 72 h of infusion. The sum excretion from infused toadfish was relatively efficient, accounting for over 40% of the infused dose by 72 h. Mechanistic knowledge of the mechanisms of toxicity of waterborne Ni in marine systems is a critical component to the development of physiologically based modeling approaches to accurately predict Ni toxicity in marine and estuarine ecosystems.

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