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幼年虹鳟鱼在慢性亚致死镉暴露期间的组织特异性镉积累、金属硫蛋白诱导以及组织锌和铜水平

Tissue-specific cadmium accumulation, metallothionein induction, and tissue zinc and copper levels during chronic sublethal cadmium exposure in juvenile rainbow trout.

作者信息

Hollis L, Hogstrand C, Wood C M

机构信息

Department of Biology, McMaster University, 1280 Main Street West, Hamilton, Ontario, L8S 4K1, Canada.

出版信息

Arch Environ Contam Toxicol. 2001 Nov;41(4):468-74. doi: 10.1007/s002440010273.

DOI:10.1007/s002440010273
PMID:11598784
Abstract

Juvenile rainbow trout, on 3% of body weight daily ration, were exposed to 0 (control) or 3 microg/L Cd (as Cd(NO3)2*4H2O) in moderately hard (140 mg/L as CaCO3), alkaline (95 mg/L as CaCO3, pH 8.0) water for 30 days. Particular attention focused on Cd burden in tissues (gills, liver, kidney, and whole body) and induction of metallothionein (MT) in gills, liver, and kidney during chronic Cd exposure. Mortality in Cd-exposed fish was minimal ( approximately 10%), and no growth effects occurred over the 30-day exposure. Cd accumulated in a time-dependent fashion to 9 times (gills), 3 times (liver), 20 times (kidney), 2 times (carcass), and 2 times (whole body) control levels by 30 days; absolute concentrations were in the order kidney > gill > liver > whole body > carcass. Tissue (gills, liver, and kidney) Zn and Cu burdens were not altered by chronic exposure to 3 microg/L Cd. MT concentrations in all tissues increased over the 30 days of Cd exposure, but the increases were much less than those of Cd on a molar binding site basis. Absolute MT concentrations were in the order liver > kidney > gill, but relative increases were greatest in kidney (fourfold), followed by gills (twofold) and liver (1.3-fold). MT levels were sufficient to bind all Cd in gill, liver, and kidney under control conditions, and after chronic Cd exposure remained sufficient in liver and kidney, but not in gills. Total metal levels (Cd + Zn + Cu) greatly exceeded MT binding capacity in all tissues under all conditions.

摘要

将体重3%作为日食量的幼年虹鳟鱼,置于硬度适中(以碳酸钙计为140毫克/升)、呈碱性(以碳酸钙计为95毫克/升,pH值8.0)的水中,分别暴露于0(对照)或3微克/升的镉(以硝酸镉四水合物形式存在)环境中30天。特别关注慢性镉暴露期间组织(鳃、肝脏、肾脏和全身)中的镉负荷以及鳃、肝脏和肾脏中金属硫蛋白(MT)的诱导情况。镉暴露组鱼的死亡率极低(约10%),且在30天的暴露期内未出现生长效应。到30天时,镉以时间依赖性方式累积至对照组水平的9倍(鳃)、3倍(肝脏)、20倍(肾脏)、2倍(鱼体)和2倍(全身);绝对浓度顺序为肾脏>鳃>肝脏>全身>鱼体。长期暴露于3微克/升镉不会改变组织(鳃、肝脏和肾脏)中的锌和铜负荷。在镉暴露的30天内,所有组织中的MT浓度均有所增加,但从摩尔结合位点来看,增加幅度远小于镉的增加幅度。MT的绝对浓度顺序为肝脏>肾脏>鳃,但相对增加幅度最大的是肾脏(四倍),其次是鳃(两倍)和肝脏(1.3倍)。在对照条件下,MT水平足以结合鳃、肝脏和肾脏中的所有镉,慢性镉暴露后,肝脏和肾脏中的MT水平仍足以结合镉,但鳃中则不然。在所有条件下,所有组织中的总金属水平(镉+锌+铜)均大大超过MT的结合能力。

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