Multi-Omics Analysis Reveals the Toxicity of Polyvinyl Chloride Microplastics toward BEAS-2B Cells

被引:2
|
作者
Liu, Chengzhi [1 ]
Chen, Shuang [1 ]
Chu, Jiangliang [1 ]
Yang, Yifan [1 ]
Yuan, Beilei [1 ]
Zhang, Huazhong [2 ,3 ]
机构
[1] Nanjing Tech Univ, Coll Safety Sci & Engn, Nanjing 210009, Peoples R China
[2] Nanjing Med Univ, Dept Emergency Med, Affiliated Hosp 1, Nanjing 210029, Peoples R China
[3] Nanjing Med Univ, Inst Poisoning, Nanjing 211100, Peoples R China
基金
中国国家自然科学基金;
关键词
microplastics; polyvinyl chloride; BEAS-2B; multi-omics; lipid metabolism; MEDIATED CROSSTALK; LIPID-METABOLISM; MAPK; APOPTOSIS; DISEASE; MECHANISMS; AUTOPHAGY; PATHWAYS; PLASTICS; DRUGS;
D O I
10.3390/toxics12060399
中图分类号
X [环境科学、安全科学];
学科分类号
08 ; 0830 ;
摘要
Polyvinyl chloride microplastics (PVC-MPs) are microplastic pollutants widely present in the environment, but their potential risks to human lung health and underlying toxicity mechanisms remain unknown. In this study, we systematically analyzed the effects of PVC-MPs on the transcriptome and metabolome of BEAS-2B cells using high-throughput RNA sequencing and untargeted metabolomics technologies. The results showed that exposure to PVC-MPs significantly reduced the viability of BEAS-2B cells, leading to the differential expression of 530 genes and 3768 metabolites. Further bioinformatics analyses showed that PVC-MP exposure influenced the expression of genes associated with fluid shear stress, the MAPK and TGF-beta signaling pathways, and the levels of metabolites associated with amino acid metabolism. In particular, integrated pathway analysis showed that lipid metabolic pathways (including glycerophospholipid metabolism, glycerolipid metabolism, and sphingolipid metabolism) were significantly perturbed in BEAS-2B cells following PVC-MPs exposure. This study provides new insights and targets for a deeper understanding of the toxicity mechanism of PVC-MPs and for the prevention and treatment of PVC-MP-associated lung diseases.
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页数:14
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