Mesnage Robin, Biserni Martina, Wozniak Eva, Xenakis Theodoros, Mein Charles A, Antoniou Michael N
Gene Expression and Therapy Group, King's College London, Faculty of Life Sciences & Medicine, Department of Medical and Molecular Genetics, Guy's Hospital, 8th Floor, Tower Wing, Great Maze Pond, London SE1 9RT, United Kingdom.
Genome Centre, Barts and the London School of Medicine and Dentistry, John Vane Science Centre, London EC1M 6BQ, United Kingdom.
Toxicol Rep. 2018 Aug 11;5:819-826. doi: 10.1016/j.toxrep.2018.08.005. eCollection 2018.
Use and thus exposure to quizalofop-p-ethyl, isoxaflutole, mesotrione and glyphosate, which are declared as active principles in commercial formulations of herbicides, is predicted to rapidly increase in coming years in an effort to overcome the wide-spread appearance of glyphosate-resistant weeds, especially in fields where glyphosate-tolerant genetically modified crops are cultivated in the USA. Thus, there is an urgent need for an evaluation of metabolic effects of new pesticide ingredients used to replace glyphosate. As the liver is a primary target of chemical pollutant toxicity, we have used the HepaRG human liver cell line as a model system to assess the toxicological insult from quizalofop-p-ethyl, isoxaflutole, mesotrione and glyphosate by determining alterations in the transcriptome caused by exposure to three concentrations of each of these compounds, including a low environmentally relevant dose. RNA-seq data were analysed with HISAT2, StringTie and Ballgown. Quizalofop-p-ethyl was found to be the most toxic of the pesticide ingredients tested, causing alterations in gene expression that are associated with pathways involved in fatty acid degradation and response to alcoholism. Isoxaflutole was less toxic, but caused detectable changes in retinol metabolism and in the PPAR signalling pathway at a concentration of 1 mM. ToxCast data analysis revealed that isoxaflutole activated PPAR gamma receptor and pregnane X responsive elements in reporter gene assays. Glyphosate and mesotrione caused subtle changes in transcriptome profiles, with too few genes altered in their function to allow a reliable pathway analysis. In order to explore the effects of glyphosate in greater depth and detail, we undertook a global metabolome profiling. This revealed a decrease in free long chain fatty acids and polyunsaturated fatty acid levels at the lowest concentration (0.06 μM) of glyphosate, although no effects were detected at the two higher concentrations tested, perhaps suggesting a non-linear dose response. This surprising result will need to be confirmed by additional studies. Overall, our findings contribute to filling the knowledge gap regarding metabolic toxicity that can potentially arise from exposure to these four herbicide active principles.
精喹禾灵、异恶唑草酮、硝磺草酮和草甘膦在除草剂商业配方中被列为活性成分,预计在未来几年其使用量以及由此导致的接触量将迅速增加,以应对草甘膦抗性杂草的广泛出现,尤其是在美国种植耐草甘膦转基因作物的田地中。因此,迫切需要评估用于替代草甘膦的新农药成分的代谢效应。由于肝脏是化学污染物毒性的主要靶器官,我们使用HepaRG人肝细胞系作为模型系统,通过确定暴露于这四种化合物的三种浓度(包括低环境相关剂量)所引起的转录组变化,来评估精喹禾灵、异恶唑草酮、硝磺草酮和草甘膦的毒理学损伤。RNA测序数据用HISAT2、StringTie和Ballgown进行分析。结果发现,在所测试的农药成分中,精喹禾灵毒性最大,会导致与脂肪酸降解和酒精中毒反应相关途径的基因表达发生改变。异恶唑草酮毒性较小,但在1 mM浓度下会引起视黄醇代谢和PPAR信号通路的可检测变化。ToxCast数据分析显示,异恶唑草酮在报告基因检测中激活了PPARγ受体和孕烷X反应元件。草甘膦和硝磺草酮引起转录组图谱发生细微变化,功能改变的基因太少,无法进行可靠的途径分析。为了更深入、详细地探究草甘膦的影响,我们进行了全代谢组分析。结果显示,在草甘膦最低浓度(0.06 μM)下,游离长链脂肪酸和多不饱和脂肪酸水平降低,尽管在测试的两个较高浓度下未检测到影响,这可能表明存在非线性剂量反应。这一惊人结果需要更多研究来证实。总体而言,我们的研究结果有助于填补关于接触这四种除草剂活性成分可能产生的代谢毒性方面的知识空白。