Hollis L, McGeer J C, McDonald D G, Wood C M
Department of Biology, McMaster University, ON, L8S 4K1, Hamilton, Canada.
Aquat Toxicol. 2000 Nov;51(1):93-105. doi: 10.1016/s0166-445x(00)00099-0.
The objectives of the study were to determine the physiological and toxicological effects of chronic cadmium exposure on juvenile rainbow trout in soft water. Particular attention focused on acclimation, on comparison to an earlier hard water study, and on whether a gill surface binding model, originally developed in dilute soft water, could be applied in this water quality to fish chronically exposed to Cd. Juvenile rainbow trout, on 3% of body weight daily ration, were exposed to 0 (control), 0.07, and 0.11 microg l(-1) Cd [as Cd(NO(3))(2).4H(2)O] in synthetic soft water (hardness=20 mg l(-1) as CaCO(3), alkalinity=15 mg l(-1) as CaCO(3), pH 7.2) for 30 days. Mortality was minimal for all treatments (up to 14% for 0.11 microg l(-1) Cd). No significant effects of chronic Cd exposure were seen in growth rate, swimming performance (stamina), routine O(2) consumption, or whole body/plasma ion levels. In contrast to the hard water study, no acclimation occurred in either exposure group in soft water, with no significant increases in 96-h LC(50) values. Cadmium accumulated in a time-dependent fashion to twice the control levels in the gills and only marginally in the liver by 30 days. No significant Cd accumulation occurred in the gall bladder or whole body. Cadmium uptake/turnover tests were run using radioactive 109Cd for acute (3 h) exposures. Saturation of the gills occurred for control fish but not for Cd-exposed fish when exposed to up to 36 microg l(-1) Cd for 3 h. Cd-exposed trout accumulated less 'new' Cd in their gills compared to controls and they internalized less 109Cd than control fish. This effect of lowered Cd uptake by the gills of acclimated trout was earlier seen for the fish acclimated to 10 microg l(-1) Cd in hard water. The affinity of the gill for Cd was greater in hard water (logK(Cd-gill)=7.6) than in soft water (logK(Cd-gill)=7.3) but the number of binding sites (B(max)=0.20 microg g(-1) gill) was similar in both media. In addition, there was a shift in affinity of the gill for Cd (i.e. lowered logK(Cd-gill)) and increased B(max) with chronic Cd exposure in both soft water and hard water. We conclude that the present gill modelling approach (i.e. acute gill surface binding model or Biotic Ligand Model) does work for soft and hard water exposures but there are complications when applying the model to fish chronically exposed to cadmium.
本研究的目的是确定长期镉暴露对软水中幼年虹鳟鱼的生理和毒理学影响。特别关注了驯化情况、与早期硬水研究的比较,以及最初在稀释软水中建立的鳃表面结合模型是否可应用于长期暴露于镉的这种水质中的鱼类。以体重3%的日食量投喂的幼年虹鳟鱼,在合成软水中(硬度 = 20 mg/L 以碳酸钙计,碱度 = 15 mg/L 以碳酸钙计,pH 7.2)暴露于0(对照)、0.07和0.11 μg/L的镉[以硝酸镉·4水合物形式存在]30天。所有处理组的死亡率都很低(0.11 μg/L镉处理组最高为14%)。长期镉暴露对生长速率、游泳性能(耐力)、常规耗氧量或全身/血浆离子水平均无显著影响。与硬水研究不同,软水中的两个暴露组均未发生驯化,96小时半数致死浓度(LC50)值也未显著增加。到30天时,镉以时间依赖性方式在鳃中积累至对照水平的两倍,而在肝脏中仅略有积累。胆囊和全身均未发生显著的镉积累。使用放射性109Cd进行急性(3小时)暴露的镉摄取/周转试验。对照鱼在暴露于高达36 μg/L镉3小时时鳃发生饱和,但镉暴露组的鱼未饱和。与对照组相比,镉暴露的鳟鱼鳃中积累的“新”镉较少,并且它们摄取的109Cd比对照鱼少。这种经驯化的鳟鱼鳃对镉摄取降低的效应,在硬水中适应于10 μg/L镉的鱼中更早出现。鳃对镉 的亲和力在硬水中(logK(镉 - 鳃)= 7.6)比在软水中(logK(镉 - 鳃)= 7.3)更大,但两种介质中的结合位点数(Bmax = 0.20 μg/g鳃)相似。此外,在软水和硬水中,长期镉暴露都会导致鳃对镉的亲和力发生变化(即logK(镉 - 鳃)降低)以及Bmax增加。我们得出结论,目前的鳃建模方法(即急性鳃表面结合模型或生物配体模型)在软水和硬水暴露中均有效,但将该模型应用于长期暴露于镉的鱼类时存在一些复杂情况。