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: 2011
• 资助国家: 加拿大
• 起止时间: 2011-01-01 至 2012-12-31
• 项目状态: 已结题
• 来源: https://www.nserc-crsng.gc.ca/ase-oro/Details-Detailles_eng.asp?id=482027
• 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.

本研究旨在研究虹鳟慢性亚致死镍和铜中毒的生理机制，从初始的体内平衡破坏到最终的适应。调查将跟踪金属从水中被吸收到各种组织（鳃、肝、肾、肌肉）时发生的生理破坏，并随着组织中金属浓度的增加，区分能够解毒和储存（或消除）金属的细胞防御系统和与积累的金属发生反应并被其破坏的细胞元素。一种将生物积累的金属划分为不同的细胞池的方法，代表潜在的有毒形式的金属和解毒形式的金属，将与生理反应联系起来。将评估一系列生理反应（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，主要的破坏将发生在离子稳态和活性氧（ROS）的产生中，并且这些破坏将在暴露期间以双相方式发生，首先是离子稳态，然后是ROS。根据这一假设，暴露早期金属的摄取预计会破坏离子调节（Cu干扰Na和Ni干扰Mg）。这是可以预测的，因为从研究急性金属暴露的生理效应的数据显示对离子调节的影响。在暴露的第二阶段，大量的金属将渗透到细胞中，随着浓度的上升，解毒机制将不堪重负，ROS将产生。在这种情况下的预测是，ROS诱导的病理生理将与毒性池中金属亚细胞部分的增加直接相关。镍和铜在离子调节和组织生物积累方面的结果截然不同，但在细胞分配和ROS的产生方面存在相似之处。这些研究旨在了解鱼类在适应金属暴露时的生理反应、损伤修复和调整；这些数据对更好地管理金属对环境的影响具有社会经济意义。