Polystyrene microplastic exposure disrupts mitochondrial pathways and nuclear processes in primary intestinal epithelial cells
- 1The University of Notre Dame Australia
Abstract
Microplastics are pervasive environmental pollutants that pose a growing concern for human health. Oral ingestion is a common route of human microplastic exposure, yet the proteomic response of the gut epithelium to microplastics remains unclear. This study aimed to investigate the cellular effects of pristine and artificially digested microplastic exposure in primary rat duodenal epithelial cells using untargeted proteomics. Cells were exposed to pristine or digested 0.5 um polystyrene microplastics at 10 or 100 ug/mL for 72 hours and were then analyzed by tandem liquid chromatography and mass spectrometry (LC-MS). Proteins that were both significantly different in intensity compared to controls, with a threshold change of 1.3 or greater, were considered to be differentially expressed. This criterion identified 41 differentially expressed proteins after 100 ug/mL pristine MP exposure, with 19 downregulated and 21 upregulated. Following exposure to 100 ug/mL digested MP, only 3 differentially expressed proteins were upregulated and 7 were down regulated, demonstrating the impact of microplastic physicochemistry. FGSEA pathway analysis revealed that 270 Reactome pathways were significantly altered following microplastic exposure in either condition at both concentrations. These pathways contributed to functional domains including protein synthesis, DNA replication, cell cycle control and aerobic respiration. Overall, microplastic exposure was associated with upregulated mitochondrial respiration, and downregulation of nuclear-related processes including DNA synthesis, transcription and cell proliferation. This study provides targets for future investigation (mitochondria and nucleus) and emphasizes the need to consider biological and environmental conditions for in vitro models of microplastic exposure.
Related
- Progerin disrupts intestinal epithelial homeostasis by impairing mitochondrial metabolism and absorptive enterocyte maturation
- Waste-to-Nanomedicine: Scalable Production of Apple Pomace Nanovesicle-Enriched Fractions as Nanocarriers for Hydrophobic Bioactives at the Intestinal Epithelial Interface
- Betaine restores OPA1-mediated mitochondrial fusion in alveolar epithelial type 2 cells and ameliorates hyperoxic lung injury in newborn mice
- When do mitochondrial processes become instructive during pluripotent-state transitions.
- TAMs-derived exosomal PD-L1 drives mitochondrial dysfunction and aberrant fatty acid oxidation via PGC-1α/PPARα axis to promote peritoneal metastasis in epithelial ovarian cancer
BibTeX
@misc{sofield2026polystyrene,
title = {{Polystyrene microplastic exposure disrupts mitochondrial pathways and nuclear processes in primary intestinal epithelial cells}},
author = {C. E. Sofield and A. M. Gorecki and L. S. Chiu and C. Anyaegbu and R. Anderton},
howpublished = {bioRxiv},
year = {2026},
month = sep,
doi = {10.64898/2026.09.22.753448},
url = {https://www.biorxiv.org/content/10.64898/2026.09.22.753448v1},
note = {CC BY},
}
RIS
TY - UNPB
TI - Polystyrene microplastic exposure disrupts mitochondrial pathways and nuclear processes in primary intestinal epithelial cells
AU - C. E. Sofield
AU - A. M. Gorecki
AU - L. S. Chiu
AU - C. Anyaegbu
AU - R. Anderton
PY - 2026
DA - 2026/09/22
PB - bioRxiv
DO - 10.64898/2026.09.22.753448
UR - https://www.biorxiv.org/content/10.64898/2026.09.22.753448v1
AB - Microplastics are pervasive environmental pollutants that pose a growing concern for human health. Oral ingestion is a common route of human microplastic exposure, yet the proteomic response of the gut epithelium to microplastics remains unclear. This study aimed to investigate the cellular effects of pristine and artificially digested microplastic exposure in primary rat duodenal epithelial cells using untargeted proteomics. Cells were exposed to pristine or digested 0.5 um polystyrene microplastics at 10 or 100 ug/mL for 72 hours and were then analyzed by tandem liquid chromatography and mass spectrometry (LC-MS). Proteins that were both significantly different in intensity compared to controls, with a threshold change of 1.3 or greater, were considered to be differentially expressed. This criterion identified 41 differentially expressed proteins after 100 ug/mL pristine MP exposure, with 19 downregulated and 21 upregulated. Following exposure to 100 ug/mL digested MP, only 3 differentially expressed proteins were upregulated and 7 were down regulated, demonstrating the impact of microplastic physicochemistry. FGSEA pathway analysis revealed that 270 Reactome pathways were significantly altered following microplastic exposure in either condition at both concentrations. These pathways contributed to functional domains including protein synthesis, DNA replication, cell cycle control and aerobic respiration. Overall, microplastic exposure was associated with upregulated mitochondrial respiration, and downregulation of nuclear-related processes including DNA synthesis, transcription and cell proliferation. This study provides targets for future investigation (mitochondria and nucleus) and emphasizes the need to consider biological and environmental conditions for in vitro models of microplastic exposure.
ER -