Pane Eric F, Haque Aziz, Goss Greg G, Wood Chris M
Department of Biology, McMaster University, Hamilton, Ontario, Canada, L8S 4K.
J Exp Biol. 2004 Mar;207(Pt 7):1249-61. doi: 10.1242/jeb.00871.
In rainbow trout (Oncorhynchus mykiss), following chronic (42 day) exposure to both 384 microg Ni l(-1) and 2034 microg Ni l(-1), Ni accumulation was greatest in the gill, kidney and plasma, with the plasma as the main sink for Ni. Indeed, trapped plasma analysis revealed that extensive loading of Ni in the plasma accounted for substantial percentages of accumulated Ni in several tissues including the liver and heart. Accumulated Ni in the gill and kidney was less dependent on plasma Ni concentration, suggesting a more intracellular accumulation of Ni in these tissues. We present evidence for a clear, persistent cost of acclimation to chronic, sublethal Ni exposure. Chronic (40-99 day) exposure to sublethal waterborne Ni (243-394 microg Ni l(-1); approximately 1% of the 96 h LC(50)) impaired the exercise physiology, but not the resting physiology, of rainbow trout. Ni acted as a limiting stressor, decreasing maximal rates of oxygen consumption (MO2,max) during strenuous exercise in trout exposed for 34 days to sublethal Ni. This drop in high-performance gas exchange was attributed mainly to a reduction in relative branchial diffusing capacity (D(rel)) caused by thickening of secondary lamellae. Morphometric analysis of the gills of chronically exposed fish revealed overall swelling of secondary lamellae, as well as hypertrophic respiratory epithelia within secondary lamellae. Additionally, contraction of the lamellar blood pillar system and narrowing of interlamellar water channels occurred, possibly contributing to decreased high-performance gas exchange. Decreased aerobic capacity persisted in fish previously exposed to nickel despite a clean-water exposure period of 38 days and an almost complete depuration of gill Ni, suggesting that extrabranchial mechanisms of chronic Ni toxicity may also be important. Chronic impairment of such a dynamically active and critical organ as the gill may depress the overall fitness of a fish by impairing predator avoidance, prey capture and migration success with obvious environmental implications.
在虹鳟鱼(Oncorhynchus mykiss)中,经过42天长期暴露于384微克/升和2034微克/升的镍环境后,镍在鳃、肾脏和血浆中的积累量最大,其中血浆是镍的主要蓄积部位。实际上,截留血浆分析表明,血浆中大量的镍负荷占包括肝脏和心脏在内的多个组织中镍蓄积量的很大比例。鳃和肾脏中蓄积的镍对血浆镍浓度的依赖性较小,这表明这些组织中镍的细胞内蓄积更为明显。我们提供的证据表明,长期亚致死性镍暴露会导致明显且持续的适应性代价。长期(40 - 99天)暴露于亚致死性水体镍(243 - 394微克/升;约为96小时半数致死浓度(LC50)的1%)会损害虹鳟鱼的运动生理学,但不会影响其静止生理学。镍作为一个限制性应激源,会降低暴露于亚致死性镍34天的虹鳟鱼在剧烈运动时的最大耗氧率(MO2,max)。这种高性能气体交换的下降主要归因于次生鳃小片增厚导致的相对鳃扩散能力(D(rel))降低。对长期暴露鱼类鳃的形态计量学分析显示,次生鳃小片整体肿胀,次生鳃小片中呼吸上皮肥大。此外,鳃小片血柱系统收缩和鳃小片间水通道变窄,这可能导致高性能气体交换降低。尽管经过38天的清水暴露期且鳃中的镍几乎完全清除,但先前暴露于镍的鱼类的有氧能力仍然下降,这表明镍慢性毒性的鳃外机制可能也很重要。像鳃这样动态活跃且关键的器官受到慢性损害,可能会通过损害鱼类躲避捕食者、捕获猎物和迁徙成功的能力,从而降低鱼类的整体适应性,这对环境具有明显的影响。