Chemical Exposure and Effects in Freshwater Aquatic Species

D. Haffner
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Abstract

To protect aquatic ecosystems from stresses induced by toxic chemicals, risk models must be developed, calibrated and verified for feral populations. Although risk models require good estimates of chemical exposure (dose) and quantitative measures of effects (response), few models, if any, have been appropriately calibrated for linking dose and response in situ. It is this lack of knowledge that limits the development of strong cause-effect relationships for aquatic species. Exposure models, using quantitative biomonitoring techniques, have been developed independently from bioassay and/or biomarker systems that are used to quantify stress. The present research integrated these two approaches by comprehensively calibrating the brown bullhead (Ameiurus nebulosus) as an appropriate bioindicator of toxicological stress in aquatic ecosystems. This was achieved by integrating quantitative biomonitoring techniques with a novel, sensitive assay for genotoxicity of polynuclear aromatic hydrocarbons (PAHs). At four sites along the river, chemical exposures and the incidence of dermal papillomas and neoplastic lesions in liver tissue were quantified, along with the measurement of PAH metabolites in bile, quantification of DNA damage in erythrocytes using the alkaline single cell gel electrophoresis (Comet assay), and the quantification of changes in apoptotic processes in dermal and liver tissues of exposed fish. Field studies on metabolite formation and apoptosis were compared to laboratory investigations in order to quantify the link between PAH metabolites and genotoxicity. Bullheads were exposed to Detroit River bottom sediment and environmentally-relevant levels of a major genotoxic PAH, benzo[a]pyrene (B[a]P), and dose-response models of metabolite formation were developed in order to determine the mass of PAH chemicals that are converted to DNA active metabolites. Genotoxicity was assessed in these laboratory populations using the comet assay on erythrocytes and liver cells. We assessed the link between DNA damage and the down-regulation of apoptosis, which is characterized as one of the key initial steps of tumorogenesis. This title belongs to WERF Research Report Series ISBN: 9781843397540 (Print) ISBN: 9781780403922 (eBook)
淡水水生物种的化学暴露及其影响
为了保护水生生态系统免受有毒化学品造成的压力,必须为野生种群开发、校准和验证风险模型。虽然风险模型需要对化学接触(剂量)进行良好的估计和对影响(反应)进行定量测量,但很少有模型(如果有的话)经过适当校准,以便在现场将剂量和反应联系起来。正是这种知识的缺乏限制了水生物种因果关系的发展。使用定量生物监测技术的暴露模型已经独立于用于量化压力的生物测定和/或生物标志物系统而开发出来。本研究将这两种方法结合起来,综合校准了棕头鱼(Ameiurus nebulosus)作为水生生态系统毒理学胁迫的合适生物指标。这是通过将定量生物监测技术与一种新的、敏感的多核芳烃(PAHs)遗传毒性分析相结合来实现的。在沿河的四个地点,对化学暴露和肝脏组织中皮肤乳头瘤和肿瘤病变的发生率进行了量化,同时测量了胆汁中多环芳烃代谢物的含量,使用碱性单细胞凝胶电泳(Comet测定)对红细胞DNA损伤进行了量化,并对暴露的鱼的皮肤和肝脏组织中细胞凋亡过程的变化进行了量化。为了量化多环芳烃代谢物与遗传毒性之间的联系,将代谢物形成和凋亡的现场研究与实验室研究进行了比较。牛头鱼暴露于底特律河底沉积物和主要遗传毒性多环芳烃苯并[a]芘(B[a]P)的环境相关水平,并建立了代谢物形成的剂量反应模型,以确定转化为DNA活性代谢物的多环芳烃化学物质的质量。在这些实验室人群中使用彗星试验对红细胞和肝细胞进行遗传毒性评估。我们评估了DNA损伤与细胞凋亡下调之间的联系,细胞凋亡是肿瘤发生的关键初始步骤之一。本文属于WERF研究报告系列ISBN: 9781843397540(印刷)ISBN: 9781780403922(电子书)
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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