The long-term in vitro co-exposure of polyethylene terephthalate (PET) nanoplastics and cigarette smoke condensate exacerbates the induction of carcinogenic traits
This study examines the long-term impact of polyethylene terephthalate nanoplastics (PET-NPLs) and cigarette smoke condensate (CSC) on human lung BEAS-2B cells, focusing on key biological hallmarks of carcinogenesis. True-to-life PET-NPLs were generated from plastic water bottles and characterized t...
| Autores: | , , , , , , , |
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| Tipo de recurso: | artículo |
| Fecha de publicación: | 2025 |
| País: | España |
| Institución: | Universitat Autònoma de Barcelona |
| Repositorio: | Dipòsit Digital de Documents de la UAB |
| Idioma: | inglés |
| OAI Identifier: | oai:ddd.uab.cat:311524 |
| Acceso en línea: | https://ddd.uab.cat/record/311524 https://dx.doi.org/urn:doi:10.1016/j.jhazmat.2025.138359 |
| Access Level: | acceso abierto |
| Palabra clave: | Nanoplastics Cigarette smoke condensate Long-term co-exposure Beas-2B cells Carcinogenic traits |
| Sumario: | This study examines the long-term impact of polyethylene terephthalate nanoplastics (PET-NPLs) and cigarette smoke condensate (CSC) on human lung BEAS-2B cells, focusing on key biological hallmarks of carcinogenesis. True-to-life PET-NPLs were generated from plastic water bottles and characterized to simulate environmental exposure conditions; and a comprehensive battery of assays was employed to assess genotoxicity, cellular transformation, and invasiveness. It was observed that, compared to passage control and individual exposures, co-exposure to PET-NPLs and CSC exacerbates oxidative stress, genotoxicity, and tumorigenic transformation, as evidenced by increased DNA damage, colony formation in soft agar, and enhanced cell migration and invasion. Transcriptomic analysis revealed a shift in cellular stress regulation including the upregulation of stress-response genes, including SLC7A11, NQO1, and HSPA1A, which are linked to oxidative stress adaptation and tumor survival. At the same time, key tumor-suppressor genes, such as LOX, and FN1, were significantly downregulated, promoting cellular transformation and invasiveness. These results provide compelling evidence that the combination of PET-NPLs and CSC enhances carcinogenic traits through oxidative stress, genomic instability, and disruption of tumor-suppressive pathways. This study underscores the importance of evaluating the synergistic effects of combined environmental exposures and their implications for human health. |
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