Pane Eric F, McDonald M Danielle, Curry H Nathan, Blanchard Jonathan, Wood Chris M, Grosell Martin
Department of Biology, McMaster University, Hamilton, Ont, Canada.
Aquat Toxicol. 2006 Oct 25;80(1):70-81. doi: 10.1016/j.aquatox.2006.07.015. Epub 2006 Jul 29.
The effects of acute Ni exposure on the marine gulf toadfish (Opsanus beta) were investigated via separate exposures to waterborne nickel (Ni) and arterially infused Ni. Of the plasma electrolytes measured after 72 h of waterborne exposure (215.3 and 606.1 microM Ni in SW (salinity of 34)), only plasma [Ca2+] was significantly impacted (approximately 55% decrease at both exposure concentrations). At both exposure concentrations, plasma [Ni] was regulated for 24h, after which a linear accumulation over time occurred. Accumulation of Ni in the plasma, and in tissues in direct contact with seawater (gill, stomach, and intestine), was roughly proportional to the Ni concentration of the exposure water. Hydromineral balance in the intestinal fluid (IF) was markedly impacted, with Na(+), Cl(-), SO(4)(2-), K+, and Mg2+ concentrations elevated after 72 h of exposure to waterborne Ni. Following arterial Ni infusion (0.40 micromolNikg(-1)h(-1)), perturbation of hydromineral balance of the intestinal fluid was specific only to Na+ (significantly elevated by Ni infusion) and Mg2+ (significantly decreased by Ni infusion). Nitrogen excretion was not significantly impacted by Ni infusion. In all tissues save the kidney, Ni accumulation via infusion was only a fraction of that observed during waterborne exposures. Remarkably, the kidney Ni burden following infusion was almost identical to that resulting from both waterborne exposures, suggesting homeostatic control. Ni excretion, dominated at 24 h by extrarenal routes, was primarily a function of renal excretion by 72 h of infusion. The sum excretion from infused toadfish was relatively efficient, accounting for over 40% of the infused dose by 72 h. Mechanistic knowledge of the mechanisms of toxicity of waterborne Ni in marine systems is a critical component to the development of physiologically based modeling approaches to accurately predict Ni toxicity in marine and estuarine ecosystems.
通过分别暴露于水体镍（Ni）和动脉注射镍，研究了急性镍暴露对海湾蟾鱼（Opsanus beta）的影响。在水体暴露72小时后（盐度为34的海水中镍浓度分别为215.3和606.1微摩尔）测量的血浆电解质中，只有血浆[Ca2+]受到显著影响（两种暴露浓度下均下降约55%）。在两种暴露浓度下，血浆[Ni]在24小时内受到调节，之后随时间呈线性积累。血浆以及与海水直接接触的组织（鳃、胃和肠道）中镍的积累大致与暴露水体中的镍浓度成正比。肠道液（IF）中的水盐平衡受到显著影响，暴露于水体镍72小时后，Na+、Cl-、SO4(2-)、K+和Mg2+浓度升高。动脉注射镍（0.40微摩尔镍·千克-1·小时-1）后，肠道液水盐平衡的扰动仅特定于Na+（注射镍后显著升高）和Mg2+（注射镍后显著降低）。氮排泄未受到镍注射的显著影响。除肾脏外，所有组织通过注射积累的镍仅为水体暴露期间观察到的一小部分。值得注意的是，注射后肾脏中的镍负荷几乎与两种水体暴露后的负荷相同，表明存在稳态控制。镍排泄在24小时内以外肾途径为主，到注射72小时时主要是肾脏排泄的功能。注射蟾鱼的总排泄效率相对较高，到72小时时占注射剂量的40%以上。了解水体镍在海洋系统中的毒性机制是开发基于生理学的建模方法以准确预测镍在海洋和河口生态系统中毒性的关键组成部分。
