Abstract
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 96h (pluteus larvae) to 55 (±2.4)μgPb/L or 117 (±11)μgZn/L, representing ~70% of the EC50 for normal 72h development. Growth, unidirectional Ca uptake rates, whole body ion concentrations (Na, K, Ca, Mg), Ca2+ 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 45Ca 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 Ca2+ATPase activities increased, Ca uptake rates returned to normal intermittently, and whole body Ca levels were restored to control values by 72-96h 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 72h.
| Original language | English |
|---|---|
| Pages (from-to) | 220-229 |
| Number of pages | 10 |
| Journal | Aquatic Toxicology |
| Volume | 146 |
| DOIs | |
| State | Published - Jan 1 2014 |
Fingerprint
Keywords
- Calcification
- Echinoderm
- Embryonic development
- Lead
- Spicule
- Toxicity
- Zinc
ASJC Scopus subject areas
- Aquatic Science
- Health, Toxicology and Mutagenesis
Cite this
Sublethal mechanisms of Pb and Zn toxicity to the purple sea urchin (Strongylocentrotus purpuratus) during early development. / Tellis, Margaret S.; Lauer, Mariana M.; Nadella, Sunita; Bianchini, Adalto; Wood, Chris M.
In: Aquatic Toxicology, Vol. 146, 01.01.2014, p. 220-229.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Sublethal mechanisms of Pb and Zn toxicity to the purple sea urchin (Strongylocentrotus purpuratus) during early development
AU - Tellis, Margaret S.
AU - Lauer, Mariana M.
AU - Nadella, Sunita
AU - Bianchini, Adalto
AU - Wood, Chris M.
PY - 2014/1/1
Y1 - 2014/1/1
N2 - 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 96h (pluteus larvae) to 55 (±2.4)μgPb/L or 117 (±11)μgZn/L, representing ~70% of the EC50 for normal 72h development. Growth, unidirectional Ca uptake rates, whole body ion concentrations (Na, K, Ca, Mg), Ca2+ 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 45Ca 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 Ca2+ATPase activities increased, Ca uptake rates returned to normal intermittently, and whole body Ca levels were restored to control values by 72-96h 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 72h.
AB - 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 96h (pluteus larvae) to 55 (±2.4)μgPb/L or 117 (±11)μgZn/L, representing ~70% of the EC50 for normal 72h development. Growth, unidirectional Ca uptake rates, whole body ion concentrations (Na, K, Ca, Mg), Ca2+ 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 45Ca 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 Ca2+ATPase activities increased, Ca uptake rates returned to normal intermittently, and whole body Ca levels were restored to control values by 72-96h 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 72h.
KW - Calcification
KW - Echinoderm
KW - Embryonic development
KW - Lead
KW - Spicule
KW - Toxicity
KW - Zinc
UR - http://www.scopus.com/inward/record.url?scp=84890012277&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84890012277&partnerID=8YFLogxK
U2 - 10.1016/j.aquatox.2013.11.004
DO - 10.1016/j.aquatox.2013.11.004
M3 - Article
C2 - 24326189
AN - SCOPUS:84890012277
VL - 146
SP - 220
EP - 229
JO - Aquatic Toxicology
JF - Aquatic Toxicology
SN - 0166-445X
ER -