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首页> 外文期刊>Journal of Comparative Physiology, B. Biochemical, Systemic, and Environmental Physiology >Branchial versus intestinal silver toxicity and uptake in the marineteleost Parophrys vetulus
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Branchial versus intestinal silver toxicity and uptake in the marineteleost Parophrys vetulus

机译：鳃与肠道银毒性和在野马进鼠饲料中的毒性和摄取

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摘要

Exposure to elevated waterborne silver as AgNO3 (4.07 muM = 448 mug 1(-1)) in seawater resulted in osmoregulatory disturbance in the lemon sole (Parophrys vetulus). The main effects were increased plasma Na+ and Cl- concentrations which translated into increased plasma osmolality. Plasma Mg2+ levels were also slightly increased after 96 h exposure. Using radioisotopic flux measurements, a 50% reduction in branchial unidirectional Na+ extrusion was observed after 48 h silver exposure. By applying an intestinal perfusion approach, we were able to separate and thus quantify the intestinal contribution to the observed silver-induced physiological disturbance and internal silver accumulation. This analysis revealed that the intestinal contribution to silver-induced ionoregulatory toxicity was as high as 50-60%. In marked contrast, internal silver accumulation (in liver and kidney) was found to be derived exclusively from uptake across the gills. Drinking of silver-contaminated seawater resulted in substantial silver accumulation in the intestinal tissue (but apparently not silver uptake across the intestine), which probably explains the intestinal contribution to silver-induced physiological disturbance.
机译：在海水中暴露于升高的水性银（4.07毫米= 448杯1（-1））导致柠檬鞋底（散步序列）中的Osmoregulatory干扰。主要效应增加了血浆Na +和Cl-浓度，其转化为增加的血浆渗透压。 96小时暴露后，血浆Mg2 +水平也略微增加。使用放射性传感器通量测量，在48小时银曝光后观察到鳃单向Na +挤出的50％降低。通过施加肠灌注方法，我们能够分离，从而量化对观察到的银诱导的生理干扰和内银积累的肠道贡献。该分析显示，肠道对银诱导的离子致毒性毒性的贡献高达50-60％。在显着的对比中，发现内部银积累（在肝肾中）仅从鳃上的摄取中得到。饮用银污染的海水导致肠道组织中的大量银积累（但显然不受肠道的银色摄取），这可能解释了对银诱导的生理干扰的肠道贡献。

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