Blewett Tamzin A, Glover Chris N, Fehsenfeld Sandra, Lawrence Michael J, Niyogi Som, Goss Greg G, Wood Chris M
Department of Biology, McMaster University, Hamilton, ON L8S 4K1, Canada; Bamfield Marine Sciences Center, Bamfield, BC V0R 1B0, Canada.
Bamfield Marine Sciences Center, Bamfield, BC V0R 1B0, Canada; School of Biological Sciences, University of Canterbury, Private Bag 4800, Christchurch, New Zealand.
Aquat Toxicol. 2015 Jul;164:23-33. doi: 10.1016/j.aquatox.2015.04.010. Epub 2015 Apr 9.
In freshwater, invertebrates nickel (Ni) is considered an ionoregulatory toxicant, but its mechanism of toxicity in marine settings, and how this varies with salinity, is poorly understood. This study investigated Ni accumulation and physiological mechanisms of sub-lethal Ni toxicity in the euryhaline green crab Carcinus maenas. Male crabs were exposed to 8.2μg/L (the US EPA chronic criterion concentration for salt waters) of waterborne Ni (radiolabelled with (63)Ni) at three different salinities, 20%, 60% and 100% SW for 24h. Whole body Ni accumulation in 20% SW was 3-5 fold greater than in 60% or 100% SW, and >80% of accumulated Ni was in the carapace at all salinities. Ni also accumulated in posterior gill 8, which showed a higher accumulation in 20% SW than in other salinities, a pattern also seen at higher exposure concentrations of Ni (500 and 3000μg/L). Gill perfusion experiments revealed that Ni was taken up by both anterior and posterior gills, but in 20% SW the posterior gill 8, which performs ionoregulatory functions, accumulated more Ni than the anterior gill 5, which primarily has a respiratory function. The sub-lethal consequences of Ni exposure were investigated by placing crabs in Ni concentrations of 8.2, 500, and 3000μg/L at 20, 60 or 100% SW for 24h. In 20% SW, haemolymph Ca levels were significantly decreased by exposure to Ni concentrations of 8.2μg/L or higher, whereas Na concentrations were depressed only at 3000μg/L. Na(+)/K(+)-ATPase activity was inhibited at both 500 and 3000μg/L in gill 8, but only in 20% SW. Haemolymph K, Mg, and osmolality were unaffected throughout, though all varied with salinity in the expected fashion. These data suggest that Ni impacts ionoregulatory function in the green crab, in a gill- and salinity-dependent manner.
在淡水中,镍(Ni)被认为是一种离子调节毒物,但人们对其在海洋环境中的毒性机制以及这种机制如何随盐度变化了解甚少。本研究调查了广盐性青蟹(Carcinus maenas)中镍的积累情况以及亚致死性镍毒性的生理机制。雄性螃蟹在三种不同盐度(20%、60%和100%的海水)下暴露于8.2μg/L(美国环境保护局设定的海水慢性标准浓度)的水溶镍(用(63)Ni放射性标记)中24小时。在20%的海水中,全身镍的积累量比在60%或100%的海水中高3至5倍,并且在所有盐度下,积累的镍中超过80%存在于甲壳中。镍也在鳃8后部积累,在20%的海水中其积累量高于其他盐度,在较高镍暴露浓度(500和3000μg/L)下也观察到这种模式。鳃灌注实验表明,镍可被前鳃和后鳃摄取,但在20%的海水中,执行离子调节功能的鳃8后部比主要具有呼吸功能的前鳃5积累了更多的镍。通过将螃蟹置于20%、60%或100%海水的8.2、500和3000μg/L镍浓度下24小时,研究了镍暴露的亚致死后果。在20%的海水中,暴露于8.2μg/L或更高镍浓度会使血淋巴中的钙水平显著降低,而钠浓度仅在3000μg/L时降低。鳃8中500和3000μg/L的镍浓度均会抑制钠钾ATP酶活性,但仅在20%的海水中出现这种情况。血淋巴中的钾、镁和渗透压在整个过程中未受影响,尽管它们都以预期的方式随盐度变化。这些数据表明,镍以鳃和盐度依赖的方式影响青蟹的离子调节功能。