Wicks B J, Joensen R, Tang Q, Randall D J
Department of Zoology, University of British Columbia, 6270 University Blvd., BC, Vancouver, Canada.
Aquat Toxicol. 2002 Sep 10;59(1-2):55-69. doi: 10.1016/s0166-445x(01)00236-3.
This study tested the hypothesis that swimming exacerbates ammonia toxicity in fish. Both sub-lethal and acute toxicity testing was conducted in a swim tunnel on swimming and resting coho salmon and rainbow trout, respectively. The sub lethal tests on coho salmon also considered the compartmentalization of ammonia within the fish. Coho salmon showed a significant linear decrease in U(crit) both with increasing water ammonia (0, 0.02, 0.04 and 0.08 mg per l NH3) and increasing plasma ammonia. Data collected included plasma pH and ammonia, muscle pH and ammonia and muscle membrane potential. Based on results found in these experiments it was concluded that the reduction in swimming performance was due to both metabolic challenges as well as depolarization of white muscle. Acute toxicity testing on swimming and resting rainbow trout revealed that swimming at (60% U(crit) or approximately 2.2 body lengths/s) decreased the LC50 level from 207+/-21.99 mg N per l in resting fish to 32.38+/-10.81. The LC50 for resting fish was significantly higher than that for swimming fish. The acute value set forth by the US EPA at the same pH is 36.1 mg N per l and may not protect swimming fish. In addition the effect of water hardness on ammonia toxicity was considered. It was found that increased water calcium ameliorates ammonia toxicity in fish living in high pH water.
本研究验证了游泳会加剧鱼类氨毒性这一假设。分别在游泳通道中对游动和静止的银大麻哈鱼及虹鳟进行了亚致死和急性毒性测试。对银大麻哈鱼的亚致死测试还考虑了鱼体内氨的分布情况。随着水体氨含量(0、0.02、0.04和0.08毫克每升NH₃)增加以及血浆氨含量增加,银大麻哈鱼的临界游速(U(crit))呈显著线性下降。收集的数据包括血浆pH值和氨含量、肌肉pH值和氨含量以及肌肉膜电位。基于这些实验结果得出结论,游泳能力下降是由于代谢挑战以及白肌去极化所致。对游动和静止虹鳟的急性毒性测试表明,以(60% U(crit)或约2.2体长/秒)的速度游动会使半致死浓度(LC50)水平从静止鱼的207±21.99毫克氮每升降至32.38±10.81。静止鱼的LC50显著高于游动鱼。美国环境保护局在相同pH值下设定的急性值为36.1毫克氮每升,可能无法保护游动的鱼。此外,还考虑了水硬度对氨毒性的影响。研究发现,增加水体钙含量可减轻生活在高pH值水中鱼类的氨毒性。