Aminated polystyrene and DNA strand breaks in A549, Caco-2, THP-1 and U937 human cell lines
- PMID: 40185540
- DOI: 10.1016/j.mrgentox.2025.503865
Aminated polystyrene and DNA strand breaks in A549, Caco-2, THP-1 and U937 human cell lines
Abstract
Plastic is used extensively worldwide. However, plastic particles that are less than 1000 nm (i.e. nanoplastics) may be hazardous to human cells. Nanoplastics might be manufactured intentionally or be formed in the environment by degradation of larger plastic items. Ingestion and inhalation are the two most common routes of human exposure to nanoplastics, indicating that epithelial cells have direct exposure. However, immune cells will also interact with particles during tissue inflammation. An assessment of published studies suggests that polystyrene (PS) particles generate higher levels of DNA damage in immune cells compared to epithelial cells, although it has not been formally studied under the same experimental condition. To investigate this, we assessed cytotoxicity, oxidative stress and DNA strand breaks in lung epithelial (A549) cells, intestinal epithelial (Caco-2) cells, and two monocytes (THP-1 and U937) after exposure to amine-functionalized polystyrene particles (PS-NH2) with declared particle size of 240 nm. No cytotoxicity or intracellular reactive oxygen species production were found at concentrations up to 200 µg/mL. Exposure to PS-NH2 was associated with glutathione depletion in A549 cells. However, there was no increase in the level of DNA strand breaks, measured by the comet assay, in any of the cell lines under standard assay conditions. Diethyl maleate treatment was used to render cells susceptible to oxidative stress. By itself, diethyl maleate treatment led to approximately 50 % glutathione depletion and increased DNA strand breaks, but additional DNA damage was not observed in cells by PS-NH2 exposure in A549, Caco-2, THP-1 and U937 cells.
Keywords: Comet assay; Nanoplastic; Oxidative stress; Polystyrene; Susceptible model.
Copyright © 2025 The Authors. Published by Elsevier B.V. All rights reserved.
Conflict of interest statement
Declaration of Competing Interest The authors report no declarations of interest.
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