4.7 Article

Sublethal mechanisms of Pb and Zn toxicity to the purple sea urchin (Strongylocentrotus purpuratus) during early development

Journal

AQUATIC TOXICOLOGY
Volume 146, Issue -, Pages 220-229

Publisher

ELSEVIER
DOI: 10.1016/j.aquatox.2013.11.004

Keywords

Echinoderm; Lead; Zinc; Embryonic development; Toxicity; Spicule; Calcification

Funding

  1. International Development Research Centre (IDRC, Ottawa, Canada)
  2. Canada Research Chair Program
  3. 'Conselho Nacional de Desenvolvirnento Cientifico e Tecnologico' (CNPq), Brasilia, DF, Brazil [304430/2009-9]
  4. International Research Chair Program from IDRC
  5. CAPES (Coordenacao de Aperfeicoamento de Pessoal do Ensino Superior, Brasilia, DF, Brazil)
  6. 'Programa Ciencias do Mar'
  7. two NSERC CRD
  8. International Zinc Association (IZA)
  9. International Lead Zinc Research Organization (ILZRO)
  10. Nickel Producers Environmental Research Association (NiPERA)
  11. International Copper Association (ICA)
  12. Copper Development Association (CDA)

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In order to understand sublethal mechanisms of lead (Pb) and zinc (Zn) toxicity, developing sea urchins were exposed continuously from 3 h post-fertilization (eggs) to 96 h (pluteus larvae) to 55 (+/- 2.4) mu g Pb/L or 117 (+/- 11) mu g Zn/L, representing similar to 70% of the EC50 for normal 72 h development. Growth, unidirectional Ca uptake rates, whole body ion concentrations (Na, K, Ca, Mg), Ca (2+) ATPase activity, and metal bioaccumulation were monitored every 12 h over this period. Pb exhibited marked bioaccumulation whereas Zn was well-regulated, and both metals had little effect on growth, measured as larval dry weight, or on Na, K, or Mg concentrations. Unidirectional Ca uptake rates (measured by Ca-45 incorporation) were severely inhibited by both metals, resulting in lower levels of whole body Ca accumulation. The greatest disruption occurred at gastrulation. Ca2+ ATPase activity was also significantly inhibited by Zn but not by Pb. Interestingly, embryos exposed to Pb showed some capacity for recovery, as Ca(2+)ATPase activities increased, Ca uptake rates returned to normal intermittently, and whole body Ca levels were restored to control values by 72-96 h of development. This did not occur with Zn exposure. Both Pb and Zn rendered their toxic effects through disruption of Ca homeostasis, though likely through different proximate mechanisms. We recommend studying the toxicity of these contaminants periodically throughout development as an effective way to detect sublethal effects, which may not be displayed at the traditional toxicity test endpoint of 72 h. (C) 2013 Elsevier B.V. All rights reserved.

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