# Comparative Metabolomic Approaches to Nanoplastic Toxicity in Mammalian and Aquatic Systems

**Authors:** Junhyuk Lee, Hyeonji Jang, Boyun Kim, Jewon Jung

PMC · DOI: 10.3390/ijms27010050 · International Journal of Molecular Sciences · 2025-12-20

## TL;DR

This paper reviews how nanoplastics affect metabolism in mammals and aquatic species, revealing shared pathways like lipid and amino acid metabolism disruption.

## Contribution

The study systematically compares metabolomic responses to nanoplastics in mammals and aquatic systems, identifying common disrupted pathways.

## Key findings

- Nanoplastics disrupt lipid metabolism, TCA cycle, and amino acid metabolism in both mammalian and aquatic systems.
- Polystyrene and polyethylene terephthalate nanoplastics induce oxidative and inflammatory stress in mammalian liver and intestine.
- Aquatic species show similar metabolic disturbances in gills, liver, and brain due to nanoplastic exposure.

## Abstract

Nanoplastics (NPs), emerging contaminants originating from the degradation of larger plastics, have raised significant environmental and health concerns due to their ability to penetrate biological barriers and disturb cellular homeostasis. Exposure to NPs has been shown to induce oxidative stress, mitochondrial dysfunction, and inflammatory responses in both mammalian and aquatic systems, ultimately leading to metabolic imbalance. Metabolomics, a comprehensive analytical approach focusing on small-molecule metabolites, provides a direct reflection of these biochemical alterations and offers critical insights into the mechanisms underlying NP-induced toxicity. This review summarizes recent metabolomic studies investigating nanoplastic toxicity across mammalian and aquatic organisms, highlighting commonly perturbed pathways such as lipid metabolism, arachidonic acid metabolism, the tricarboxylic acid (TCA) cycle, and amino acid metabolism. These disruptions indicate that NPs impair energy production, lipid regulation, and redox balance. In mammals, polystyrene and polyethylene terephthalate nanoplastics have been shown to alter hepatic and intestinal metabolism and induce oxidative and inflammatory stress, while in aquatic species, similar metabolic disturbances occur in the gills, liver, and brain. Collectively, the evidence emphasizes metabolomics as a powerful approach for elucidating the molecular basis of nanoplastic toxicity and suggests that integration with other omics techniques is essential for comprehensive risk assessment and mechanistic understanding.

## Full-text entities

- **Diseases:** mitochondrial dysfunction (MESH:D028361), inflammatory (MESH:D007249), Toxicity (MESH:D064420)
- **Chemicals:** NP (-), arachidonic acid (MESH:D016718), TCA (MESH:D014233), polyethylene terephthalate (MESH:D011093), amino acid (MESH:D000596), lipid (MESH:D008055), polystyrene (MESH:D011137)

## Full text

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## Figures

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## References

174 references — full list in the complete paper: https://tomesphere.com/paper/PMC12785257/full.md

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Source: https://tomesphere.com/paper/PMC12785257