Liang Yanshan, Tang Zhi, Jiang Yousheng, Ai Chunyan, Peng Jinling, Liu Yuan, Chen Jinru, Zhang Jianqing, Cai Zongwei
Beijing Normal University-Hong Kong Baptist University United International College, Zhuhai, China; State Key Laboratory of Environmental and Biological Analysis, Department of Chemistry, Hong Kong Baptist University, Hong Kong Special Administrative Region; Shenzhen Center for Disease Control and Prevention, Shenzhen, China.
Shenzhen Center for Disease Control and Prevention, Shenzhen, China; Department of Environmental and Occupational Health, School of Public Health, Guangdong Medical University, Dongguan, China.
Environ Int. 2020 Oct;143:105984. doi: 10.1016/j.envint.2020.105984. Epub 2020 Jul 23.
Dioxins, a group of persistent organic pollutants, have been proved to correlate with ranges of diseases by activating the aryl hydrocarbon receptor (AhR). However, previous dioxin toxicity studies primarily focused on the activation of AhR with signaling pathways at gene and protein levels. The investigation of underlying mechanisms at the metabolic level is still necessary. In this study, serum samples of 48 and 47 healthy participants with the highest and lowest dioxin levels based on quartile distribution of the serum dioxin concentrations of 215 male adults were selected for metabolomics analysis by using liquid chromatography coupled with orbitrap high-resolution mass spectrometry to investigate dioxin-related metabolic responses. The identified potential biomarkers included acylcarnitines, fatty acids and derivatives, glycerophospholipids, etc. suggested that metabolic pathways such as fatty acid β-oxidation, essential fatty acid metabolism, arachidonic acid metabolism, glycerophospholipid and sphingolipid metabolism and purine metabolism were disturbed by dioxin exposure. The results indicated that people with high dioxin exposure levels were at the potential health risks of inflammation, liver and cardiovascular diseases. The metabolic findings may help understand the link between dioxin exposure and the diseases.
二噁英是一类持久性有机污染物，已被证明可通过激活芳烃受体（AhR）与多种疾病相关联。然而，以往的二噁英毒性研究主要集中在基因和蛋白质水平上AhR与信号通路的激活。在代谢水平上对潜在机制的研究仍然是必要的。在本研究中，根据215名男性成年人血清二噁英浓度的四分位数分布，选择了48名二噁英水平最高和47名二噁英水平最低的健康参与者的血清样本，采用液相色谱-轨道阱高分辨率质谱联用技术进行代谢组学分析，以研究与二噁英相关的代谢反应。鉴定出的潜在生物标志物包括酰基肉碱、脂肪酸及其衍生物、甘油磷脂等，表明脂肪酸β-氧化、必需脂肪酸代谢、花生四烯酸代谢、甘油磷脂和鞘脂代谢以及嘌呤代谢等代谢途径受到二噁英暴露的干扰。结果表明，二噁英暴露水平高的人群存在炎症、肝脏和心血管疾病的潜在健康风险。这些代谢研究结果可能有助于理解二噁英暴露与疾病之间的联系。
