Mechanisms of acute and chronic waterborne nickel toxicity in the freshwater cladoceran, Daphnia magna

Eric F. Pane, Clint Smith, James C. Mcgeer, Chris M. Wood

Research output: Contribution to journalArticle

99 Citations (Scopus)

Abstract

We present evidence that Mg2+ antagonism is one mechanism for acute toxicity of waterborne Ni to Daphnia magna. Acutely, adult D. magna were exposed to either control or 694 μg Ni L-1 as NiS04 in moderately soft water (45 mg L-1 as CaC03; background Ni ≅ 1 μg Ni L-1) for 48 h without feeding. Chronically, adults were exposed to either control or 131 μug Ni L-1 for 14 days (fed exposure). These concentrations were approximately 65% and 12%, respectively, of the measured 48-h LC50 (1068, μg Ni L-1) for daphnid neonates in this water quality. The clearest effect of Ni exposure was on Mg2+ homeostasis, as whole- body [Mg2+] was significantly decreased both acutely and chronically by 18%. Additionally, unidirectional Mg2+ uptake rate (measured with the stable isotope 26Mg) was significantly decreased both acutely and chronically by 49 and 47%, respectively, strongly suggesting that Ni is toxic to D. magna due at least in part to Mg2+ antagonism. No impact was observed on the whole-body concentrations or unidirectional uptake rates of Ca2+ during either acute or chronic Ni exposure, while only minor effects were seen on Na+ and Cl- balance. No acute toxic effect was seen on respiratory parameters, as both oxygen consumption rate (M02) and whole-body hemoglobin concentration ([Hb]) were conserved. Chronically, however, Ni impaired respiratory function, as both M02 and [Hb] were significantly reduced by 31 and 68%, respectively. Acutely, Ni accumulation was substantial, rising to a plateau between 24 and 48 h of approximately 15 μg g-1 wet weight - an increase of approximately 25-fold over control concentrations. Mechanisms of acute toxicity of Ni in D. magnadifferfrom those in fish; itis likely that such mechanistic differences also exist for other metals.

Original languageEnglish
Pages (from-to)4382-4389
Number of pages8
JournalEnvironmental Science and Technology
Volume37
Issue number19
DOIs
StatePublished - Oct 1 2003

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Nickel
Toxicity
nickel
antagonism
Poisons
toxicity
neonate
Hemoglobin
homeostasis
hemoglobin
oxygen consumption
Isotopes
Fish
Water quality
Hemoglobins
stable isotope
Metals
plateau
Oxygen
fold

ASJC Scopus subject areas

  • Environmental Engineering
  • Environmental Science(all)
  • Environmental Chemistry

Cite this

Mechanisms of acute and chronic waterborne nickel toxicity in the freshwater cladoceran, Daphnia magna. / Pane, Eric F.; Smith, Clint; Mcgeer, James C.; Wood, Chris M.

In: Environmental Science and Technology, Vol. 37, No. 19, 01.10.2003, p. 4382-4389.

Research output: Contribution to journalArticle

Pane, Eric F. ; Smith, Clint ; Mcgeer, James C. ; Wood, Chris M. / Mechanisms of acute and chronic waterborne nickel toxicity in the freshwater cladoceran, Daphnia magna. In: Environmental Science and Technology. 2003 ; Vol. 37, No. 19. pp. 4382-4389.
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abstract = "We present evidence that Mg2+ antagonism is one mechanism for acute toxicity of waterborne Ni to Daphnia magna. Acutely, adult D. magna were exposed to either control or 694 μg Ni L-1 as NiS04 in moderately soft water (45 mg L-1 as CaC03; background Ni ≅ 1 μg Ni L-1) for 48 h without feeding. Chronically, adults were exposed to either control or 131 μug Ni L-1 for 14 days (fed exposure). These concentrations were approximately 65{\%} and 12{\%}, respectively, of the measured 48-h LC50 (1068, μg Ni L-1) for daphnid neonates in this water quality. The clearest effect of Ni exposure was on Mg2+ homeostasis, as whole- body [Mg2+] was significantly decreased both acutely and chronically by 18{\%}. Additionally, unidirectional Mg2+ uptake rate (measured with the stable isotope 26Mg) was significantly decreased both acutely and chronically by 49 and 47{\%}, respectively, strongly suggesting that Ni is toxic to D. magna due at least in part to Mg2+ antagonism. No impact was observed on the whole-body concentrations or unidirectional uptake rates of Ca2+ during either acute or chronic Ni exposure, while only minor effects were seen on Na+ and Cl- balance. No acute toxic effect was seen on respiratory parameters, as both oxygen consumption rate (M02) and whole-body hemoglobin concentration ([Hb]) were conserved. Chronically, however, Ni impaired respiratory function, as both M02 and [Hb] were significantly reduced by 31 and 68{\%}, respectively. Acutely, Ni accumulation was substantial, rising to a plateau between 24 and 48 h of approximately 15 μg g-1 wet weight - an increase of approximately 25-fold over control concentrations. Mechanisms of acute toxicity of Ni in D. magnadifferfrom those in fish; itis likely that such mechanistic differences also exist for other metals.",
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AB - We present evidence that Mg2+ antagonism is one mechanism for acute toxicity of waterborne Ni to Daphnia magna. Acutely, adult D. magna were exposed to either control or 694 μg Ni L-1 as NiS04 in moderately soft water (45 mg L-1 as CaC03; background Ni ≅ 1 μg Ni L-1) for 48 h without feeding. Chronically, adults were exposed to either control or 131 μug Ni L-1 for 14 days (fed exposure). These concentrations were approximately 65% and 12%, respectively, of the measured 48-h LC50 (1068, μg Ni L-1) for daphnid neonates in this water quality. The clearest effect of Ni exposure was on Mg2+ homeostasis, as whole- body [Mg2+] was significantly decreased both acutely and chronically by 18%. Additionally, unidirectional Mg2+ uptake rate (measured with the stable isotope 26Mg) was significantly decreased both acutely and chronically by 49 and 47%, respectively, strongly suggesting that Ni is toxic to D. magna due at least in part to Mg2+ antagonism. No impact was observed on the whole-body concentrations or unidirectional uptake rates of Ca2+ during either acute or chronic Ni exposure, while only minor effects were seen on Na+ and Cl- balance. No acute toxic effect was seen on respiratory parameters, as both oxygen consumption rate (M02) and whole-body hemoglobin concentration ([Hb]) were conserved. Chronically, however, Ni impaired respiratory function, as both M02 and [Hb] were significantly reduced by 31 and 68%, respectively. Acutely, Ni accumulation was substantial, rising to a plateau between 24 and 48 h of approximately 15 μg g-1 wet weight - an increase of approximately 25-fold over control concentrations. Mechanisms of acute toxicity of Ni in D. magnadifferfrom those in fish; itis likely that such mechanistic differences also exist for other metals.

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