McMaster University, Department of Biology, Hamilton, Ontario L8S 4K1, Canada; Bamfield Marine Sciences Centre, Bamfield, British Columbia V0R 1B0, Canada.
Bamfield Marine Sciences Centre, Bamfield, British Columbia V0R 1B0, Canada; Instituto de Ciências Biológicas, Universidade Federal do Rio Grande (FURG), 96203-900 Rio Grande, Rio Grande do Sul, Brazil.
Aquat Toxicol. 2014 Jan;146:220-9. doi: 10.1016/j.aquatox.2013.11.004. Epub 2013 Nov 12.
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.
为了理解铅（Pb）和锌（Zn）毒性的亚致死机制，从受精后 3 小时（卵）到 96 小时（幼体），连续暴露于 55（±2.4）μgPb/L 或 117（±11）μgZn/L 的海胆发育中，这代表了正常 72 小时发育的 EC50 的~70%。在此期间，每隔 12 小时监测生长、单向 Ca 摄取率、全身体离子浓度（Na、K、Ca、Mg）、Ca(2+)ATP 酶活性和金属生物积累。Pb 表现出明显的生物积累，而 Zn 则得到很好的调节，这两种金属对生长（以幼虫干重衡量）或 Na、K 或 Mg 浓度几乎没有影响。单向 Ca 摄取率（通过（45）Ca 掺入测量）被这两种金属严重抑制，导致全身 Ca 积累水平降低。最大的干扰发生在原肠胚形成期。Zn 但不是 Pb 显著抑制 Ca(2+)ATP 酶活性。有趣的是，暴露于 Pb 的胚胎显示出一定的恢复能力，因为 Ca(2+)ATP 酶活性增加，Ca 摄取率间歇性地恢复正常，并且整个身体的 Ca 水平在发育的 72-96 小时内恢复到对照值。Zn 暴露时则不会出现这种情况。Pb 和 Zn 通过破坏 Ca 稳态发挥其毒性作用，尽管可能通过不同的直接机制。我们建议在整个发育过程中定期研究这些污染物的毒性，作为检测亚致死效应的有效方法，这些效应可能不会在 72 小时的传统毒性测试终点显示出来。
