Integration of transcriptomics and metabolomics reveal cytotoxic mechanisms of Polyethylene terephthalate microplastics in BEAS-2B cells.
Autor: | Chu J; College of Safety Science and Engineering, Nanjing Tech University, Nanjing, Jiangsu 210009, China., Yang Y; College of Safety Science and Engineering, Nanjing Tech University, Nanjing, Jiangsu 210009, China., Zhang K; College of Safety Science and Engineering, Nanjing Tech University, Nanjing, Jiangsu 210009, China., Fu Y; College of Safety Science and Engineering, Nanjing Tech University, Nanjing, Jiangsu 210009, China., Yuan B; College of Safety Science and Engineering, Nanjing Tech University, Nanjing, Jiangsu 210009, China. Electronic address: yuanbeilei@163.com. |
---|---|
Jazyk: | angličtina |
Zdroj: | Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association [Food Chem Toxicol] 2024 Nov 21, pp. 115125. Date of Electronic Publication: 2024 Nov 21. |
DOI: | 10.1016/j.fct.2024.115125 |
Abstrakt: | Polyethylene terephthalate microplastics (PET-MPs) have emerged as significant environmental pollutants with potential health risks. This study investigates the cytotoxic effects of PET-MPs on BEAS-2B lung epithelial cells through integrated transcriptomic and metabolomic analyses. The results of the CCK8 assay showed a reduction in the viability of BEAS-2B cells following continuous exposure to PET-MPs. Transcriptomic analysis identified 1,412 differentially expressed genes (DEGs) mainly enriched in apoptosis and extracellular matrix organization processes. Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis revealed that these DEGs are predominantly involved in the PI3K-Akt, TNF, and MAPK signaling pathways. Metabolomic analysis identified 2,869 differentially expressed metabolites (DEMs), mainly associated with pyrimidine, arginine, proline, and β-alanine metabolism pathways. Multi-omics analysis indicated that PET-MPs primarily disrupt lipid metabolism, which may lead to an increased risk of apoptosis. We hypothesize that PET-MPs affect lipid metabolism by up-regulating the ANGPTL4 gene, thereby promoting cellular apoptosis. This study reveals the mechanisms of PET-MPs toxicity, emphasizing the potential risks they pose to human health. Competing Interests: Declaration of Competing Interest ☒ The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper. (Copyright © 2024. Published by Elsevier Ltd.) |
Databáze: | MEDLINE |
Externí odkaz: |