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The use of non-targeted metabolomics to assess the toxicity of bifenthrin to juvenile Chinook salmon (Oncorhynchus tshawytscha).
Aquatic Toxicology ( IF 4.5 ) Pub Date : 2020-05-23 , DOI: 10.1016/j.aquatox.2020.105518
Jason T Magnuson 1 , Marissa Giroux 1 , Zachary Cryder 1 , Jay Gan 1 , Daniel Schlenk 2
Affiliation  

An increase in urban and agricultural application of pyrethroid insecticides in the San Francisco Bay Estuary and Sacramento San Joaquin Delta has raised concern for the populations of several salmonids, including Chinook salmon (Oncorhynchus tshawytscha). Bifenthrin, a type I pyrethroid, is among the most frequently detected pyrethroids in the Bay-Delta watershed, with surface water concentrations often exceeding chronic toxicity thresholds for several invertebrate and fish species. To better understand the mechanisms of bifenthrin-induced neurotoxicity, juvenile Chinook salmon were exposed to concentrations of bifenthrin previously measured in the Delta. Non-targeted metabolomic profiles were used to identify transcriptomic changes in the brains of bifenthrin-exposed fish. Pathway analysis software predicted increased apoptotic, inflammatory, and reactive oxygen species (ROS) responses in Chinook following exposure to 0.15 and 1.50 μg/L bifenthrin for 96 h. These responses were largely driven by reduced levels of inosine, hypoxanthine, and guanosine. Subsequently, in the brain, the expression of caspase 3, a predominant effector for apoptosis, was significantly upregulated following exposure to 1.50 μg/L bifenthrin. This data suggests that metabolites involved in inflammatory and apoptotic responses, as well as those involved in maintaining proper neuronal function may be disrupted following sublethal exposure to bifenthrin and further suggests that additional population studies should focus on behavioral responses associated with impaired brain function.



中文翻译:

使用非靶向代谢组学评估联苯菊酯对幼稚的奇努克鲑鱼(Oncorhynchus tshawytscha)的毒性。

旧金山湾河口和萨克拉曼多圣华金河三角洲的拟除虫菊酯类杀虫剂在城市和农业上的使用增加,引起了对包括奇努克鲑鱼(Oncorhynchus tshawytscha)在内的几种鲑鱼种群的关注。)。联苯菊酯(一种类型的拟除虫菊酯)是在湾三角洲流域中最常被检测到的拟除虫菊酯,其地表水浓度经常超过几种无脊椎动物和鱼类的慢性毒性阈值。为了更好地了解联苯菊酯诱导的神经毒性机制,奇努克鲑鱼被暴露在三角洲地区先前测得的联苯菊酯浓度下。非靶向代谢组学谱用于鉴定暴露于联苯菊酯的鱼脑中的转录组变化。途径分析软件预测,暴露于0.15和1.50μg/ L联苯菊酯96小时后,奇努克族人的凋亡,炎症和活性氧(ROS)反应增加。这些反应很大程度上是由于肌苷,次黄嘌呤和鸟嘌呤水平降低。随后,在大脑中半胱天冬酶3(一种主要的凋亡效应子)在暴露于1.50μg/ L联苯菊酯后显着上调。该数据表明,与联苯菊酯亚致死接触后,与炎症和凋亡反应有关的代谢产物以及与维持正常神经元功能有关的代谢产物可能会被破坏,并且进一步表明,其他人群研究应集中在与脑功能受损相关的行为反应上。

更新日期:2020-05-23
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