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Mechanisms of Genotoxicity Induced by Environmental Mutagens—Focus on Nanoparticles and Micro/Nanoplastics

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Toxicology".

Deadline for manuscript submissions: 30 November 2026 | Viewed by 1012

Editors


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Guest Editor
Group of Mutagenesis, Universitat Autònoma de Barcelona, 08193 Cerdanyola del Vallès, Spain
Interests: genotoxicity; nanoplastics; biomarkers; DNA damage; nanotoxicology
Special Issues, Collections and Topics in MDPI journals

E-Mail Website
Guest Editor
Group of Mutagenesis, Universitat Autònoma de Barcelona, 08193 Cerdanyola del Valles, Spain
Interests: genotoxicity; nanoplastics; biomarkers; DNA damage; nanotoxicology

Special Issue Information

Dear Colleagues,

Environmental pollutants continue to raise pressing concerns for both ecosystems and human health. Among these, nanoparticles and micro/nanoplastics have emerged as contaminants of particular interest; however, the molecular mechanisms underlying their genotoxic potential remain insufficiently understood. This Special Issue of the International Journal of Molecular Sciences (IJMS) seeks to gather original research and reviews that advance our knowledge of how such agents interact with biological systems and contribute to DNA damage, chromosome alterations, and genome instability, or other related molecular alterations.

We especially welcome studies evaluating different methods and tools for genotoxicity assessment, introducing new experimental methodologies, or investigating emerging environmental contaminants with potential genotoxic effects. Also, contributions identifying biomarkers or clarifying molecular pathways linking exposure to harmful outcomes are highly valued.

As IJMS is a journal of molecular science, we remind authors that purely clinical or exclusively model-based studies fall outside the journal’s scope. Nonetheless, clinical or model studies that integrate biomolecular experiments are strongly encouraged. This Special Issue aims to foster dialogue, share innovative approaches, and inspire new strategies to better understand and mitigate the risks posed by environmental mutagens.

Dr. Ricard Marcos
Dr. Susana Pastor
Guest Editors

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Keywords

  • genotoxicity
  • DNA damage
  • chromosome damage
  • DNA repair
  • comet assay
  • micronucleus assay
  • mechanisms
  • environmental pollutants
  • micro/nanoplastics
  • nanoparticles

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Published Papers (1 paper)

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Research

18 pages, 1917 KB  
Article
Long-Term PET-Nanoplastic Exposure Alters DNA Damage Response Capacity in BEAS-2B Human Bronchial Epithelial Cells
by Michelle Morataya-Reyes, Aliro Villacorta, Raquel Egea, Joan Martín-Pérez, Javier Gutiérrez-García, Susana Pastor, Ricard Marcos and Alba Hernández
Int. J. Mol. Sci. 2026, 27(11), 5031; https://doi.org/10.3390/ijms27115031 - 2 Jun 2026
Viewed by 501
Abstract
Chronic inhalation exposure to nanoplastics, specifically polyethylene terephthalate (PET) nanoplastics (PET-NPLs) is an emerging health concern, yet the long-term consequences for genomic stability and DNA damage response (DDR) capacity in bronchial epithelial cells remain poorly characterized. For this study, human bronchial epithelial BEAS-2B [...] Read more.
Chronic inhalation exposure to nanoplastics, specifically polyethylene terephthalate (PET) nanoplastics (PET-NPLs) is an emerging health concern, yet the long-term consequences for genomic stability and DNA damage response (DDR) capacity in bronchial epithelial cells remain poorly characterized. For this study, human bronchial epithelial BEAS-2B cells were continuously exposed to PET-NPLs for over 20 weeks, after which elevated basal DNA genotoxic damage was observed, as assessed by the alkaline comet assay. In addition, a broad transcriptional suppression of the DDR, with 27 of 84 profiled genes involved in DDR showing reduced expression relative to passage-matched control was observed. The suppressed genes span ATM/ATR checkpoint signaling, homologous recombination (HR), base excision repair (BER), nucleotide excision repair (NER), and apoptotic pathways. To determine whether chronic PET-NPL exposure altered susceptibility to acute genotoxic challenge in a damage-type-specific manner, cells were treated with methyl methanesulfonate (MMS), ultraviolet-C (UV-C) radiation, or bleomycin. While MMS and UV-C induced comparable levels of DNA damage in control and PET-exposed cells, bleomycin produced significantly greater damage in PET-exposed cells, indicating selective sensitization to doble-strand breaks (DSB)-type and oxidative genotoxic insults. Transcriptional profiling during bleomycin challenge identified 18 DDR genes with relatively higher expression in PET-exposed cells compared to passage-matched controls, encompassing HR, BER, ATM/ATR signaling, the Fanconi anemia pathway, and apoptosis. Furthermore, PET-exposed cells retained significantly higher residual DNA damage after 3 h of bleomycin challenge, indicating a persistent early repair deficit. Together, these findings suggest that chronic PET-NPL exposure specifically compromises the bronchial epithelial DDR, with potential implications for long-term genomic stability in respiratory epithelia subjected to nanoplastic inhalation. Full article
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