Suppr超能文献

代谢组学和脂质组学研究揭示多溴联苯醚-47 对乳腺癌小鼠的影响。

Metabolomics and lipidomics study unveils the impact of polybrominated diphenyl ether-47 on breast cancer mice.

机构信息

State Key Laboratory of Environmental and Biological Analysis, Department of Chemistry, Hong Kong Baptist University, Hong Kong Special Administrative Region, China.

State Key Laboratory of Environmental and Biological Analysis, Department of Chemistry, Hong Kong Baptist University, Hong Kong Special Administrative Region, China; State Key Laboratory of Chemical Oncogenomics, Graduate School at Shenzhen, Tsinghua University, Shenzhen, Guangdong, China.

出版信息

J Hazard Mater. 2020 May 15;390:121451. doi: 10.1016/j.jhazmat.2019.121451. Epub 2019 Oct 13.

Abstract

Polybrominated diphenyl ether-47 (BDE-47) is a congener of polybrominated diphenyl ethers (PBDEs) and relates to different health risks. However, in vivo study of the association between BDE-47 and breast cancer was scarce. In this study, we performed in vivo exposure of BDE-47 to breast cancer nude mice and conducted mass spectrometry-based metabolomics and lipidomics analysis to investigate the metabolic changes in mice. Results showed that the tumor sizes were positively associated with the dosage of BDE-47. Metabolomics and lipidomics profiling analysis indicated that BDE-47 induced significant alterations of metabolic pathways in livers, including glutathione metabolism, ascorbate and aldarate metabolism, and lipids metabolism, etc. The upregulations of phosphatidylcholines (PCs) and phosphatidylethanolamines (PEs) suggested the membrane remodeling, and the downregulations of Lyso-PCs and Lyso-PEs might be associated with the tumor growth. Targeted metabolomics analysis revealed that BDE-47 inhibited fatty acid β-oxidation (FAO) and induced incomplete FAO. The inhibition of FAO and downregulation of PPARγ would contribute to inflammation, which could promote tumor growth. In addition, BDE-47 elevated the expression of the cytokines TNFRSF12A, TNF-α, IL-1β and IL-6, and lowered the cytokines SOCS3 and the nuclear receptor PPARα. The changes of cytokines and receptor may contribute to the tumor growth of mice.

摘要

多溴二苯醚-47(BDE-47)是多溴二苯醚(PBDEs)的同系物,与不同的健康风险有关。然而,体内研究 BDE-47 与乳腺癌之间的关系还很少。在这项研究中,我们对乳腺癌裸鼠进行了 BDE-47 的体内暴露,并进行了基于质谱的代谢组学和脂质组学分析,以研究小鼠的代谢变化。结果表明,肿瘤大小与 BDE-47 的剂量呈正相关。代谢组学和脂质组学分析表明,BDE-47 诱导了肝脏代谢途径的显著改变,包括谷胱甘肽代谢、抗坏血酸和醛酸代谢以及脂质代谢等。磷脂酰胆碱(PCs)和磷脂酰乙醇胺(PEs)的上调表明了膜重塑,而溶血磷脂酰胆碱(Lyso-PCs)和溶血磷脂酰乙醇胺(Lyso-PEs)的下调可能与肿瘤生长有关。靶向代谢组学分析显示,BDE-47 抑制脂肪酸β-氧化(FAO)并诱导不完全 FAO。FAO 的抑制和 PPARγ 的下调有助于炎症,从而促进肿瘤生长。此外,BDE-47 升高了细胞因子 TNFRSF12A、TNF-α、IL-1β 和 IL-6 的表达,降低了细胞因子 SOCS3 和核受体 PPARα 的表达。细胞因子和受体的变化可能有助于小鼠肿瘤的生长。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验