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首页> 外文期刊>Aquatic Toxicology >Mortality, bioaccumulation and physiological responses in juvenile freshwater mussels (Lampsilis siliquoidea) chronically exposed to copper.
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Mortality, bioaccumulation and physiological responses in juvenile freshwater mussels (Lampsilis siliquoidea) chronically exposed to copper.

机译：长期暴露于铜的少年淡水贻贝（Lampsilis siliquoidea）的死亡率，生物蓄积和生理反应。

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Several studies have indicated that the early life stages of freshwater mussels are among the most sensitive aquatic organisms to inorganic chemicals, including copper. However, little is known about the toxic mode of action and sub-lethal effects of copper exposure in this group of imperiled animals. In this study, the physiological effects of long-term copper exposure (survival, growth, copper bioaccumulation, whole-body ion content, oxygen consumption, filtration rate, ATPase activities, and biomarkers of oxidative stress) were evaluated in juvenile (6 month old) mussels (Lampsilis siliquoidea). The mussels' recovery capacity and their ability to withstand further acute copper challenge were also evaluated in secondary experiments following the 28 day exposure by assessing survival, copper bioaccumulation and whole-body ion content. Mussels chronically exposed to 2 and 12 micro g Cu/L showed significantly higher mortality than those held under control conditions (mortality 20.9, 69.9 and 12.5%, respectively), indicating that juvenile L. siliquoidea is underprotected by the U.S. Environmental Protection Agency (USEPA) biotic ligand model (BLM)-derived chronic water quality criteria (WQC) (2.18 micro g Cu/L) and the hardness-derived USEPA WQC (12.16 micro g Cu/L). Soft tissue copper burden increased equally for both copper exposures, suggesting that chronic toxicity is not associated with copper bioaccumulation. Several physiological disturbances were also observed during chronic copper exposure. Most relevant was a decrease in whole-body sodium content paralleled by an inhibition of Na+ K+-ATPase activity, indicating a metal-induced ionoregulatory disturbance. Filtration and oxygen consumption rates were also affected. Redox parameters (reactive oxygen production, antioxidant capacity against peroxyl radicals, glutathione-S-transferase (GST) activity, and glutathione (GSH) concentration) did not show clear responses, but membrane damage as lipid peroxidation (LPO) was observed in both copper exposures. Mussels previously held in control conditions or pre-exposed to 2 micro g dissolved Cu/L were able to maintain their ionic homeostasis and did not experience mortality after the 4-d recovery period. In contrast, those previously exposed to 12 micro g dissolved Cu/L exhibited 50% mortality indicating that they had already reached a 'point of no return'. Pre-exposure to copper did not influence mussel response to the copper challenge test. As observed for the chronic exposure, mortality of mussels held in the absence of copper and submitted to the challenge test was also associated with an ionoregulatory disturbance. These results indicate that ionoregulatory disruption in freshwater mussels chronically exposed to copper is the main mechanism of toxicity and that redox parameters do not appear to be useful as indicators of sub-lethal copper toxicity in these animals.
机译：多项研究表明，淡水贻贝的生命早期阶段是对包括铜在内的无机化学物质最敏感的水生生物。但是，对于这组濒危动物中铜的毒性作用方式和亚致死作用知之甚少。在这项研究中，评估了青少年（6个月大）长期接触铜的生理效应（存活，生长，铜生物富集，全身离子含量，耗氧量，过滤速率，ATPase活性和氧化应激的生物标志物）。 ）贻贝（Lampsilis siliquoidea）。在暴露28天后，还通过评估存活率，铜的生物累积量和全身离子含量，在二次实验中评估了贻贝的恢复能力及其承受进一步的急性铜挑战的能力。长期暴露于2微克和12微克铜/升的贻贝的死亡率显着高于对照条件下的死亡率（死亡率分别为20.9％，69.9和12.5％），这表明幼稚的L. siliquoidea受美国环境保护局（USEPA）的保护不足。 ）源自生物配体模型（BLM）的慢性水质标准（WQC）（2.18 micro g Cu / L）和源自硬度的USEPA WQC（12.16 micro g Cu / L）。对于两种铜暴露，软组织的铜负荷均等增加，表明慢性毒性与铜的生物蓄积无关。在慢性铜暴露期间还观察到一些生理障碍。最相关的是全身钠含量的降低，同时抑制了Na + K + -ATPase活性，这表明金属诱导的离子调节紊乱。过滤和耗氧率也受到影响。氧化还原参数（活性氧产生，抗过氧自由基的抗氧化能力，谷胱甘肽-S-转移酶（GST）活性和谷胱甘肽（GSH）浓度）没有显示明确的响应，但是在两种铜中均观察到膜的脂质过氧化（LPO）破坏曝光。先前处于对照条件下或预先暴露于2微克溶解的Cu / L中的贻贝能够维持其离子稳态，并且在恢复4天后没有死亡。相反，先前暴露于12微克溶解的Cu / L的那些则表现出50％的死亡率，表明它们已经达到“无回报点”。预先暴露于铜不会影响贻贝对铜激发试验的反应。正如长期暴露所观察到的那样，在没有铜的情况下保存并接受攻击试验的贻贝的死亡率也与离子调节紊乱有关。这些结果表明，长期暴露于铜的淡水贻贝中的离子调节破坏是毒性的主要机制，并且氧化还原参数似乎不能用作这些动物中亚致死铜毒性的指标。

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