Linking physiological mechanisms and the chronic impacts of bioaccumulated metals in aquatic organisms

将生理机制与水生生物中生物累积金属的慢性影响联系起来

• 批准号: 341276-2008
• 负责人: McGeer, James
• 金额: $ 2.31万
• 依托单位: Wilfrid Laurier University
• 依托单位国家: 加拿大
• 项目类别: Discovery Grants Program - Individual
• 财政年份: 2013
• 资助国家: 加拿大
• 起止时间: 2013-01-01 至 2014-12-31
• 项目状态: 已结题
• 来源: https://www.nserc-crsng.gc.ca/ase-oro/Details-Detailles_eng.asp?id=527243
• 关键词: Linking; physiological; mechanisms; chronic; impacts

This research program addresses the physiological mechanisms of chronic sublethal Ni and Cu toxicity in rainbow trout, from initial disruption of homeostasis to final acclimation. Investigations will follow the physiological disruption that occurs as metals are taken up from the water into various tissues (gills, liver, kidney, muscle) and, as the concentration of metal in tissues increases, distinguish between cellular defense systems that can detoxify and store (or eliminate) the metal and cellular elements that react with and are damaged by accumulated metal. A method of partitioning bioaccumulated metal into distinct cellular pools representing potentially toxic forms of metal and detoxified forms will be linked to physiological responses. A suite of physiological responses will be assessed (e.g. immune function, stress response, vitamin A metabolism, respiratory function, ion regulation and generation of reactive oxygen species (ROS)). It is hypothesized that the primary disruptions will be in ion homeostasis and in the generation of reactive oxygen species (ROS) and that these will occur in a biphasic manner during exposure, first ion homeostasis then ROS. Under this hypothesis, the uptake of metal early in the exposure is expected to disrupt ion regulation (Cu interfering with Na and Ni with Mg). This is predicted because data from studies on the physiological effects of acute metal exposure show impacts on ion regulation. In the second phase of the exposure significant amounts of metal will have permeated into cells and as concentrations rise, detoxification mechanisms will be overwhelmed and ROS will be generated. The prediction in this case is that ROS induced pathophysiology will be directly related to increases in the subcellular fraction of metal in the toxic pool. Ni and Cu are expected to show contrasting results related to ion regulation and tissue bioaccumulation but similarities in the cellular partitioning and generation of ROS. The studies are designed to understand the physiological responses, damage repair and adjustments in fish as they acclimate to metal exposure; the data will be of socio-economic relevance to better manage the impacts of metals in the environment.

本研究计划针对虹鳟鱼慢性亚致死镍和铜毒性的生理机制，从最初的破坏稳态到最终的驯化。 调查将遵循的生理中断发生的金属从水中被带到各种组织（鳃，肝，肾，肌肉），并作为金属在组织中的浓度增加，区分细胞防御系统，可以解毒和存储（或消除）的金属和细胞元素，与积累的金属反应和损坏。 将生物积累的金属分配到代表潜在有毒形式的金属和解毒形式的不同细胞池中的方法将与生理反应相关联。将评估一系列生理反应（例如免疫功能、应激反应、维生素A代谢、呼吸功能、离子调节和活性氧（ROS）的产生）。 据推测，主要的破坏将是在离子稳态和活性氧（ROS）的产生，这些将发生在一个双相的方式在暴露期间，首先离子稳态，然后ROS。 在这一假设下，在暴露早期的金属吸收预计会破坏离子调节（铜干扰钠和镁镍）。这是预测，因为从急性金属暴露的生理影响的研究数据显示离子调节的影响。在暴露的第二阶段，大量的金属将渗透到细胞中，随着浓度的升高，解毒机制将被淹没，并产生ROS。在这种情况下的预测是，活性氧诱导的病理生理学将直接相关的毒性池中的金属的亚细胞部分的增加。镍和铜预计将显示出对比的结果与离子调节和组织的生物积累，但在细胞分配和产生的ROS的相似性。 这些研究旨在了解鱼类在适应金属接触时的生理反应、损伤修复和调整;这些数据将具有社会经济意义，有助于更好地管理金属对环境的影响。