关键词: Agrochemical Aquatic toxicology Locomotor activity Neurotoxicology Oxidative stress

Mesh : Animals Zebrafish / embryology Herbicides / toxicity Embryo, Nonmammalian / drug effects Reactive Oxygen Species / metabolism Apoptosis / drug effects Larva / drug effects Oxidative Stress / drug effects Acetamides / toxicity Neurotoxicity Syndromes / etiology

来  源:   DOI:10.1016/j.ntt.2024.107369

Abstract:
Pethoxamid, a member of the chloroacetamide herbicide family, is a recently approved chemical for pre- or post-emergence weed control; however, toxicity data for sublethal effects in aquatic organisms exposed to pethoxamid are non-existent in literature. To address this, we treated zebrafish embryos/larvae to pethoxamid over a 7-day period post-fertilization and evaluated several toxicological endpoints associated with oxidative stress and neurotoxicity. Continuous pethoxamid exposure did not affect survival nor hatch success in embryos/larvae for 7 days up to 1000 μg L-1. Exposure to pethoxamid did not affect embryonic ATP-linked respiration, but it did reduce non-mitochondrial respiration at the highest concentration tested. We also noted a significant increase in both apoptosis and levels of reactive oxygen species (ROS) in larvae zebrafish following exposure to pethoxamid. Increases in apoptosis and ROS, however, were not correlated with any altered gene expression pattern for apoptotic and oxidative damage response transcripts. To assess neurotoxicity potential, we measured behavior and several transcripts implicated in neural processes in the central nervous system. While locomotor activity of larval zebrafish was affected by pethoxamid exposure (hyperactivity was observed at concentrations below 1 μg L-1, and hypoactivity was noted at higher exposures to 10 and 100 μg L-1 pethoxamid), there were no effects on steady state mRNA abundance for neurotoxicity-related transcripts tested. This data contributes to knowledge regarding exposure risks for chloroacetamide-based herbicides and is the first study investigating sublethal toxicity for this newly registered herbicide.
摘要:
聚苯醚,氯乙酰胺除草剂家族的成员,是最近批准的用于出苗前或出苗后杂草控制的化学品;然而,在文献中不存在暴露于螺草胺的水生生物的亚致死效应的毒性数据。为了解决这个问题,我们在受精后的7天内对斑马鱼胚胎/幼虫进行了治疗,并评估了与氧化应激和神经毒性相关的几个毒理学终点.持续暴露于pethoxamid不会影响7天至1000μgL-1的胚胎/幼虫的存活或孵化成功。暴露于pethoxamid并不影响胚胎ATP相关的呼吸,但在测试的最高浓度下,它确实降低了非线粒体呼吸。我们还注意到,暴露于pethoxamid后,斑马鱼幼虫的凋亡和活性氧(ROS)水平显着增加。细胞凋亡和ROS增加,然而,与凋亡和氧化损伤反应转录本的任何改变的基因表达模式无关。为了评估潜在的神经毒性,我们测量了行为和一些涉及中枢神经系统神经过程的转录本。虽然幼体斑马鱼的运动活动受到螺酰胺暴露的影响(在浓度低于1μgL-1时观察到活动过度,在较高的10和100μgL-1螺酰胺暴露时注意到活动不足),对神经毒性相关转录本的稳态mRNA丰度没有影响.该数据有助于了解基于氯乙酰胺的除草剂的暴露风险,并且是调查这种新注册的除草剂的亚致死毒性的第一项研究。
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