Toxicity of single walled carbon nanotubes to rainbow trout, (Oncorhynchus mykiss):: Respiratory toxicity, organ pathologies, and other physiological effects

Toxicity of single walled carbon nanotubes to rainbow trout, (Oncorhynchus mykiss):: Respiratory toxicity, organ pathologies, and other physiological effects
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DOI:
10.1016/j.aquatox.2007.02.003
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发表时间:
2007-05-01
期刊:
影响因子:
4.5
通讯作者:
Handy, Richard D.
Handy, Richard D.
中科院分区:
环境科学与生态学2区
文献类型:
--
作者:
Smith, Catherine J.;Shaw, Benjamin J.;Handy, Richard D.

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哺乳动物的研究引起了人们对碳纳米管(CNT)毒性的关注,但关于对水生生物的生态毒性的数据非常有限。我们描述了第一个详细的报告单壁碳纳米管(SWCNT)的毒性虹鳟鱼,使用身体系统的方法。使用溶剂(十二烷基硫酸钠,SDS)和超声处理的组合制备分散的SWCNT的储备溶液。一个半静态测试系统被用来暴露虹鳟鱼的淡水控制,溶剂控制,0.1,0.25或0.5毫克升(-1)单壁碳纳米管长达10天。SWCNT暴露导致通气率、鳃病理学(水肿、改变的粘液细胞、增生)和粘液分泌的剂量依赖性升高,其中SWCNT沉淀在鳃粘液上。在红细胞和白色细胞计数、红细胞压积、全血血红蛋白和血浆Na+或K+方面未观察到重大血液学或血液紊乱。组织金属水平(Na+、K+、Ca 2+、Cu、Zn和Co)一般不受影响。然而,观察到脑和鳃Zn或Cu的一些剂量依赖性变化(但不是组织Ca 2+),这也部分归因于溶剂。单壁碳纳米管暴露引起鳃和肠中Na+K+-ATP酶活性的统计学显著增加,但在大脑中没有。硫代巴比妥酸反应物质(TBARS)表现出剂量依赖性和统计学显着减少,特别是在鳃,脑和肝脏在单壁碳纳米管暴露相比,控制。与溶剂对照组相比,单壁碳纳米管暴露导致鳃(28%)和肝脏(18%)中总谷胱甘肽水平的统计学显著增加。在所有处理中,脑和肠中的总谷胱甘肽保持稳定。大脑中的病理学包括小脑腹侧表面上可能的小脑萎缩或小脑萎缩。暴露于SWCNT的肝细胞显示浓缩的核小体(凋亡小体)和异常核分裂的细胞。肝脏中不存在明显的脂肪变化或广泛的脂肪变性。鱼在暴露期间摄入含有SWCNT的水(推测为应激诱导的饮水),这导致肠腔中沉淀的SWCNT和肠道病理学。攻击性行为和咬鳍在实验结束时造成了一些死亡,这可能与鳃刺激和脑损伤有关,尽管溶剂也可能部分导致攻击性。总的来说,我们得出结论,单壁碳纳米管是鳟鱼的呼吸道毒物,鱼能够管理氧化应激和神经调节紊乱,但其他细胞病变引起关注的细胞周期缺陷,神经毒性,以及尚未确定的血液家园因素,可能介导的全身性病变。(c)2007 Elsevier B.V保留所有权利。
Mammalian studies have raised concerns about the toxicity of carbon nanotubes (CNTs), but there is very limited data on ecotoxicity to aquatic life. We describe the first detailed report on the toxicity of single walled carbon nanotubes (SWCNT) to rainbow trout, using a body systems approach. Stock solutions of dispersed SWCNT were prepared using a combination of solvent (sodium dodecyl sulphate, SDS) and sonication. A semi-static test system was used to expose rainbow trout to either a freshwater control, solvent control, 0.1, 0.25 or 0.5 mg l(-1) SWCNT for up to 10 days. SWCNT exposure caused a dose-dependent rise in ventilation rate, gill pathologies (oedema, altered mucocytes, hyperplasia), and mucus secretion with SWCNT precipitation on the gill mucus. No major haematological or blood disturbances were observed in terms of red and white blood cell counts, haematocrits, whole blood haemoglobin, and plasma Na+ or K+. Tissue metal levels (Na+, K+, Ca2+, Cu, Zn and Co) were generally unaffected. However some dose-dependent changes in brain and gill Zn or Cu were observed (but not tissue Ca2+), that were also partly attributed to the solvent. SWCNT exposure caused statistically significant increases in Na+K+-ATPase activity in the gills and intestine, but not in the brain. Thiobarbituric acid reactive substances (TBARS) showed dose-dependent and statistically significant decreases especially in the gill, brain and liver during SWCNT exposure compared to controls. SWCNT exposure caused statistically significant increases in the total glutathione levels in the gills (28%) and livers (18%), compared to the solvent control. Total glutatbione in the brain and intestine remained stable in all treatments. Pathologies in the brain included possible aneurisms or swellings on the ventral surface of the cerebellum. Liver cells exposed to SWCNT showed condensed nuclear bodies (apoptotic bodies) and cells in abnormal nuclear division. Overt fatty change or wide spread lipidosis was absent in the liver. Fish ingested water containing SWCNT during exposure (presumably stress-induced drinking) which resulted in precipitated SWCNT in the gut lumen and intestinal pathology. Aggressive behaviour and fin nipping caused some mortalities at the end of the experiment, which may be associated with the gill irritation and brain injury, although the solvent may also partly contributed to aggression. Overall we conclude that SWCNTs are a respiratory toxicant in trout, the fish are able to manage oxidative stress and osmoregulatory disturbances, but other cellular pathologies raise concerns about cell cycle defects, neurotoxicity, and as yet unidentified blood home factors that possibly mediate systemic pathologies. (c) 2007 Elsevier B.V All rights reserved.