Department of Pharmacology and Toxicology, Medical College of Wisconsin, Milwaukee, WI 53226, USA.
Institute of Animal Molecular Biotechnology and Department of Biotechnology, College of Life Sciences and Biotechnology, Korea University, Seoul 02841, Republic of Korea.
Sci Total Environ. 2021 Jun 1;771:145445. doi: 10.1016/j.scitotenv.2021.145445. Epub 2021 Jan 28.
The herbicide aclonifen is commonly used in agriculture. Aclonifen is toxic to experimental animals, causing developmental abnormalities, decreased energy production for survival, and impaired organogenesis. However, no studies have reported the functional defects and toxicity caused by aclonifen in embryonic development. We hypothesized that the mechanism underlying the toxicity of several herbicides in various organisms involves mitochondrial dysfunction, which subsequently promotes genotoxicity, cytotoxicity, and acute organotoxicity. In the present study, we demonstrated that mitochondrial dysfunction during development results in decreased body length, delayed yolk sac absorption, malformed spinal cord, disrupted brain and eye formation, and the activation of apoptosis in zebrafish embryos. Aclonifen induced oxidative stress by elevating the level of reactive oxygen species, causing mitochondrial damage. Likewise, impaired embryonic vascularization can promote cardiovascular disorders. In this study, we characterized the toxicity of aclonifen in a non-target organism. These findings increase our understanding of the toxicological effects of herbicides in unexpected environments.
除草剂氯苯氧酸通常用于农业。氯苯氧酸对实验动物有毒，导致发育异常、生存能量产生减少和器官发生受损。然而，尚无研究报道氯苯氧酸在胚胎发育过程中引起的功能缺陷和毒性。我们假设，几种除草剂在各种生物体中的毒性机制涉及线粒体功能障碍，随后促进遗传毒性、细胞毒性和急性器官毒性。在本研究中，我们证明了发育过程中线粒体功能障碍导致斑马鱼胚胎体长减少、卵黄囊吸收延迟、脊髓畸形、脑和眼睛形成中断以及凋亡激活。氯苯氧酸通过提高活性氧水平诱导氧化应激，导致线粒体损伤。同样，胚胎血管生成受损可促进心血管疾病。在这项研究中，我们描述了非靶标生物中氯苯氧酸的毒性。这些发现增加了我们对预期环境中除草剂毒理学效应的理解。
