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ECB-ART-43158
Aquat Toxicol 2014 Jan 01;146:220-9. doi: 10.1016/j.aquatox.2013.11.004.
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Sublethal mechanisms of Pb and Zn toxicity to the purple sea urchin (Strongylocentrotus purpuratus) during early development.

Tellis MS , Lauer MM , Nadella S , Bianchini A , Wood CM .


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In order to understand sublethal mechanisms of lead (Pb) and zinc (Zn) toxicity, developing sea urchins were exposed continuously from 3h post-fertilization (eggs) to 96 h (pluteus larvae) to 55 (±2.4) μgPb/L or 117 (±11)μgZn/L, representing ~ 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 12h 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 (45)Ca incorporation) were severely inhibited by both metals, resulting in lower levels of whole body Ca accumulation. The greatest disruption occurred at gastrulation. Ca(2+) 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.

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Genes referenced: LOC100887844 LOC581395