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Peer-reviewedCC BY-NC 4.0Science Advances

Clinically derived micro- and nanoplastic uptake drives spatiotemporally confined metabolic stress revealed by bond-selective imaging

  • Jingyuan Li1
  • Nian Liu2
  • Delong Zhang3
  • Hyeon Jeong Lee1
  1. 1College of Biomedical Engineering & Instrument Science, Key Laboratory for Biomedical Engineering of Ministry of Education, Zhejiang University, Hangzhou 310027, China.
  2. 2State Key Laboratory of Fluid Power and Mechatronic Systems & Liangzhu Laboratory, School of Mechanical Engineering, Zhejiang University, Hangzhou 310027, China.
  3. 3Zhejiang Key Laboratory of Micro-nano Quantum Chips and Quantum Control, School of Physics, Zhejiang University, Hangzhou 310027, China.
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Abstract

Although microplastics and nanoplastics (MPs/NPs) are pervasive environmental contaminants, our understanding of cellular toxicity remains incomplete, as adverse effects are often attributed to long-term intracellular accumulation, while the spatiotemporal onset of cellular damage remains poorly defined. Here, we use chemical bond–selective stimulated Raman scattering (SRS) microscopy and cell models that decouple continuous exposure from intracellular retention to directly visualize clinically derived MP/NP-cell interactions. Cellular stress occurs primarily during MP/NP exposure, accompanied by alterations in lipid droplet (LD) composition. In contrast, following extracellular removal, intracellularly retained MP/NP become largely inert, with recovery of lipid metabolism and cellular functions. Lipidomics identifies arachidonic acid (AA) as a key dysregulated metabolite, and SRS imaging further reveals transient, spatially confined AA enrichment in MP/NP–proximal LDs during uptake. Phospholipid coating of MP/NP attenuates LD alterations and cytotoxicity while preserving particle internalization, establishing uptake-driven metabolic stress, rather than long-term intracellular retention, as a primary source of MP/NP–induced damage.

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Cite

BibTeXRIS
BibTeX
@article{li2026clinically,
  title = {{Clinically derived micro- and nanoplastic uptake drives spatiotemporally confined metabolic stress revealed by bond-selective imaging}},
  author = {Jingyuan Li and Nian Liu and Delong Zhang and Hyeon Jeong Lee},
  journal = {Science Advances},
  year = {2026},
  month = nov,
  doi = {10.1126/sciadv.aee7712},
  url = {https://www.science.org/doi/abs/10.1126/sciadv.aee7712},
  note = {CC BY-NC 4.0},
}
RIS
TY  - JOUR
TI  - Clinically derived micro- and nanoplastic uptake drives spatiotemporally confined metabolic stress revealed by bond-selective imaging
AU  - Jingyuan Li
AU  - Nian Liu
AU  - Delong Zhang
AU  - Hyeon Jeong Lee
PY  - 2026
DA  - 2026/11/04
JO  - Science Advances
DO  - 10.1126/sciadv.aee7712
UR  - https://www.science.org/doi/abs/10.1126/sciadv.aee7712
AB  - Although microplastics and nanoplastics (MPs/NPs) are pervasive environmental contaminants, our understanding of cellular toxicity remains incomplete, as adverse effects are often attributed to long-term intracellular accumulation, while the spatiotemporal onset of cellular damage remains poorly defined. Here, we use chemical bond–selective stimulated Raman scattering (SRS) microscopy and cell models that decouple continuous exposure from intracellular retention to directly visualize clinically derived MP/NP-cell interactions. Cellular stress occurs primarily during MP/NP exposure, accompanied by alterations in lipid droplet (LD) composition. In contrast, following extracellular removal, intracellularly retained MP/NP become largely inert, with recovery of lipid metabolism and cellular functions. Lipidomics identifies arachidonic acid (AA) as a key dysregulated metabolite, and SRS imaging further reveals transient, spatially confined AA enrichment in MP/NP–proximal LDs during uptake. Phospholipid coating of MP/NP attenuates LD alterations and cytotoxicity while preserving particle internalization, establishing uptake-driven metabolic stress, rather than long-term intracellular retention, as a primary source of MP/NP–induced damage.
SN  - 2375-2548
ER  -