Morgan Tammie P, Grosell Martin, Playle Richard C, Wood Chris M
Department of Biology, McMaster University, Hamilton, Ont., Canada.
Aquat Toxicol. 2004 Jan 7;66(1):55-72. doi: 10.1016/j.aquatox.2003.07.003.
The pattern of gill silver accumulation in rainbow trout during waterborne silver exposure has been reported to be unusual, reaching a peak in the first few hours of silver exposure followed by a marked decline with continued exposure. The potential causes of the pattern were investigated. Rainbow trout (1-5g) were exposed in a static system to 110mAg labeled AgNO(3) at a total concentration of 1.92microg Agl(-1) for 24h in synthetic soft water. Periodically throughout the exposure, gill and body 110mAg accumulation, gill and body 24Na uptake (from which whole body Na(+) uptake was calculated), gill Na(+)K(+)-ATPase activity, plus water silver (total and dissolved), Cl(-) and total organic carbon (TOC) concentrations were measured. Gill silver levels rapidly increased, peaked at 3h of exposure and then decreased until a plateau was reached at 12h of exposure. Body (minus gills) silver levels increased steadily over the exposure period until 18h of exposure. Whole body Na(+) uptake decreased, was maximally inhibited by 3h of exposure but recovered by 12h despite continued silver exposure. Gill Na(+)K(+)-ATPase activity was not inhibited until 5h of exposure. The water dissolved silver concentration declined by approximately 70% over the 24h exposure period and the TOC content of the water increased over three-fold during the first 2h of exposure. There was a decrease in the calculated contribution of Ag(+) (from 20.9 to 2.5%) and an increase in the calculated contribution of Ag-TOC complexes (from 77 to 97.3%) to the total water silver concentration over the first 2h of exposure. Apical silver uptake into the gills decreased over the initial 2.5h of exposure while basolateral silver export out of the gills to the body remained constant throughout the exposure. The results of this study suggest that: (1) physiological regulation of silver movement may explain the pattern of gill silver accumulation observed in rainbow trout, although not by a mechanism coupled to Na(+)K(+)-ATPase inhibition as originally proposed; (2) alternatively or additionally, a decreased bioavailability of silver, due to the static exposure conditions, may explain the pattern of gill accumulation; (3) the early inhibition of whole body Na(+) uptake observed during silver exposure occurs via a mechanism other than Na(+)K(+)-ATPase inhibition; and (4) gill silver accumulation may be an appropriate endpoint for biotic ligand modeling.
据报道,虹鳟鱼在水体银暴露期间鳃中银的积累模式不同寻常,在银暴露的最初几个小时达到峰值,随后随着持续暴露而显著下降。对这种模式的潜在原因进行了研究。将虹鳟鱼(1 - 5克)在静态系统中暴露于总浓度为1.92微克/升的110mAg标记的硝酸银中,在合成软水中暴露24小时。在整个暴露过程中定期测量鳃和鱼体的110mAg积累量、鳃和鱼体的24Na摄取量(据此计算全身Na+摄取量)、鳃Na+K+-ATP酶活性,以及水体中的银(总银和溶解银)、Cl-和总有机碳(TOC)浓度。鳃银水平迅速升高,在暴露3小时时达到峰值,然后下降,直到暴露12小时时达到平稳状态。鱼体(不包括鳃)银水平在暴露期间稳步上升,直到暴露18小时。全身Na+摄取量下降,在暴露3小时时受到最大抑制,但尽管银持续暴露,在12小时时恢复。鳃Na+K+-ATP酶活性直到暴露5小时才受到抑制。在24小时的暴露期间,水体中溶解银浓度下降了约70%,并且在暴露的前2小时内水体的TOC含量增加了三倍多。在暴露的前2小时内,计算得出的Ag+对总水体银浓度的贡献降低(从20.9%降至2.5%),而Ag-TOC络合物的贡献增加(从77%增至97.3%)。在暴露的最初2.5小时内,鳃顶端对银的摄取减少,而在整个暴露过程中,鳃基底外侧向鱼体的银输出保持恒定。本研究结果表明:(1)银移动的生理调节可能解释了虹鳟鱼中观察到的鳃银积累模式,尽管并非如最初所提出的通过与Na+K+-ATP酶抑制相关的机制;(2)作为一种替代或补充解释,由于静态暴露条件导致银的生物可利用性降低,可能解释鳃积累模式;(3)在银暴露期间观察到的全身Na+摄取的早期抑制是通过Na+K+-ATP酶抑制以外的机制发生的;(4)鳃银积累可能是生物配体模型的一个合适终点。