Pane Eric F, Haque Aziz, Wood Chris M
Department of Biology, McMaster University, 1280 Main St. West, Hamilton, Ont., Canada L8S 4K1.
Aquat Toxicol. 2004 Jul 30;69(1):11-24. doi: 10.1016/j.aquatox.2004.04.009.
In moderately hard Lake Ontario water (approximately 140 mg L(-1) as CaCO3) waterborne Ni (9.7-10.7 mg Ni L(-1)) is acutely toxic to adult rainbow trout (Oncorhynchus mykiss) exclusively via branchial mechanisms. Ventilation in resting trout (evaluated using a ventilatory masking technique) was adversely affected, as ventilation rate (VR), ventilation volume (VG), opercular stroke volume (VSV) and resting oxygen consumption (MO2) were all increased, and oxygen extraction efficiency (U%) decreased over 48 h of Ni exposure. Extensive gill Ni accumulation (41-fold over control levels) during 82 h of waterborne Ni exposure resulted in marked ultrastructural damage to the respiratory epithelium of the gill, including swelling of the secondary lamellae evidenced by changes to both the lamellar region (increased secondary lamellar tissue volume (VSL/V(LR), and to the secondary lamellae themselves (increased volume of tissue lying outside the pillar system (VOPS/VSL). Additionally, decreased lamellar height and increased lamellar width indicated a reduction in lamellar surface area available for gas diffusion. The relative diffusing capacity of experimental fish was only 59% of that of control fish. Infusion of Ni into the blood, achieving a similar time course and magnitude of plasma [Ni] elevation to that during waterborne exposure, failed to elicit any signs of respiratory toxicity typically diagnostic of acute, high level waterborne Ni exposure. Infusion of Ni into the blood for 96 h resulted in only minor accumulation of Ni in the gill, suggesting that acute Ni-induced respiratory toxicity is related to accumulation of high levels of Ni in the gill from the water. Additionally, infusion of Ni into the bloodstream led to significant extrabranchial Ni accumulation only in the kidney. White muscle, heart, liver, stomach, and intestine did not significantly accumulate Ni following infusion into the bloodstream and trapped plasma analysis revealed that, with the exception of the kidney, a substantial portion of Ni accumulated in tissues following infusion could be accounted for by extracellular (blood-bound) Ni.
在安大略湖中等硬度的水中（碳酸钙含量约为140毫克/升），水溶态镍（9.7 - 10.7毫克镍/升）对成年虹鳟（Oncorhynchus mykiss）具有急性毒性，且仅通过鳃部机制产生影响。静息状态下的虹鳟的通气（使用通气掩盖技术评估）受到不利影响，在镍暴露的48小时内，通气率（VR）、通气量（VG）、鳃盖冲程容积（VSV）和静息耗氧量（MO2）均增加，而氧提取效率（U%）降低。在水溶态镍暴露82小时期间，鳃中镍大量积累（比对照水平高41倍），导致鳃呼吸上皮出现明显的超微结构损伤，包括次生鳃小片肿胀，这通过鳃小片区域（次生鳃小片组织体积增加（VSL/V(LR)）以及次生鳃小片本身（柱系统外组织体积增加（VOPS/VSL））的变化得以证明。此外，鳃小片高度降低和宽度增加表明可用于气体扩散的鳃小片表面积减少。实验鱼的相对扩散能力仅为对照鱼的59%。向血液中注入镍，使血浆[Ni]升高的时间进程和幅度与水溶态暴露期间相似，但未能引发任何通常可诊断为急性、高浓度水溶态镍暴露的呼吸毒性迹象。向血液中注入镍96小时仅导致鳃中镍的少量积累，这表明急性镍诱导的呼吸毒性与水中高浓度镍在鳃中的积累有关。此外，向血液中注入镍仅导致肾脏中出现明显的鳃外镍积累。注入血液后，白肌、心脏、肝脏、胃和肠道并未显著积累镍，截留血浆分析表明，除肾脏外，注入后组织中积累的大部分镍可由细胞外（与血液结合的）镍来解释。
