Chu Jiangliang, Yang Yifan, Zhang Keyu, Fu Yiping, Yuan Beilei
College of Safety Science and Engineering, Nanjing Tech University, Nanjing, Jiangsu, 210009, China.
College of Safety Science and Engineering, Nanjing Tech University, Nanjing, Jiangsu, 210009, China.
Food Chem Toxicol. 2025 Jan;195:115125. doi: 10.1016/j.fct.2024.115125. Epub 2024 Nov 22.
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 1412 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 2869 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.
聚对苯二甲酸乙二酯微塑料（PET-MPs）已成为具有潜在健康风险的重要环境污染物。本研究通过综合转录组学和代谢组学分析，研究了PET-MPs对BEAS-2B肺上皮细胞的细胞毒性作用。CCK8检测结果显示，连续暴露于PET-MPs后，BEAS-2B细胞的活力降低。转录组分析鉴定出1412个差异表达基因（DEGs），主要富集于凋亡和细胞外基质组织过程。京都基因与基因组百科全书（KEGG）通路分析表明，这些DEGs主要参与PI3K-Akt、TNF和MAPK信号通路。代谢组分析鉴定出2869个差异表达代谢物（DEMs），主要与嘧啶、精氨酸、脯氨酸和β-丙氨酸代谢途径相关。多组学分析表明，PET-MPs主要扰乱脂质代谢，这可能导致细胞凋亡风险增加。我们假设PET-MPs通过上调ANGPTL4基因影响脂质代谢，从而促进细胞凋亡。本研究揭示了PET-MPs的毒性机制，强调了它们对人类健康构成的潜在风险。
