Center for Environmental and Human Toxicology, Department of Physiological Sciences, College of Veterinary Medicine, University of Florida, Gainesville, FL 32611, USA.
Center for Environmental and Human Toxicology, Department of Physiological Sciences, College of Veterinary Medicine, University of Florida, Gainesville, FL 32611, USA; Universidade Federal de São Paulo, Instituto de Ciências Ambientais, Químicas e Farmacêuticas, Campus Diadema, Brazil.
Neurotoxicol Teratol. 2024 Jul-Aug;104:107369. doi: 10.1016/j.ntt.2024.107369. Epub 2024 Jul 2.
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. 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, and hypoactivity was noted at higher exposures to 10 and 100 μg L 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.
苯噻草胺是氯乙酰胺类除草剂家族的一员，是一种最近批准的用于芽前或芽后除草的化学物质；然而，在文献中，没有关于水生生物接触苯噻草胺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 7 天内用苯噻草胺处理斑马鱼胚胎/幼虫，并评估了与氧化应激和神经毒性相关的几个毒理学终点。在 7 天内，胚胎/幼虫在 1000μg/L 以下的连续苯噻草胺暴露不会影响其存活率或孵化成功率。苯噻草胺暴露不会影响胚胎的 ATP 连接呼吸，但它确实降低了在测试的最高浓度下的非线粒体呼吸。我们还注意到，在暴露于苯噻草胺后，幼鱼斑马鱼的细胞凋亡和活性氧 (ROS) 水平显著增加。然而，细胞凋亡和 ROS 的增加与凋亡和氧化损伤反应转录物的任何改变的基因表达模式无关。为了评估神经毒性潜力，我们测量了行为和几个与中枢神经系统神经过程相关的转录本。虽然幼鱼斑马鱼的运动活性受到苯噻草胺暴露的影响（在低于 1μg/L 的浓度下观察到过度活跃，在更高浓度的 10 和 100μg/L 苯噻草胺暴露下观察到低活性），但测试的神经毒性相关转录本的稳态 mRNA 丰度没有受到影响。这一数据有助于了解氯乙酰胺类除草剂的暴露风险，也是首次研究这种新注册除草剂的亚致死毒性。
