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Clinically derived micro- and nanoplastics uptake drives spatiotemporally confined metabolic stress revealed by bond-selective imaging
Summary
Scientists watched, in real time, what happens when tiny plastic particles enter human cells—and found that the real damage happens during the moment of uptake, not from plastic sitting inside cells long-term. Once cells stopped being exposed to new particles, they actually recovered, even with plastic still inside them. This suggests that limiting ongoing exposure to microplastics may matter more than worrying about plastic that's already accumulated in our bodies, and it points to possible ways (like special coatings) to make plastics less harmful in the future.
Abstract Although microplastics and nanoplastics (MP/NP) 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 employ 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. Importantly, 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 primary source of MP/NP-induced damage.