# Mechanistic insights into the size-dependent bioaccumulation and phytotoxicity of polyethylene microplastics in tomato seedlings

**Authors:** Yuanzhou Xu, Xueqing Chen, Youxin Xu, Jie Liu, Wenxia Yang, Wei Wei, Bo Zheng, Chunlei Li

PMC · DOI: 10.3389/fpls.2026.1786469 · Frontiers in Plant Science · 2026-02-18

## TL;DR

This study shows that tiny polyethylene microplastics (1–50 μm) cause the most harm to tomato seedlings, severely affecting growth and triggering oxidative stress.

## Contribution

The study reveals a mechanistic shift in toxicity based on microplastic size, showing that smaller particles cause more severe effects through oxidative stress rather than hormonal disruption.

## Key findings

- Micro-sized polyethylene particles (1–50 μm) caused the most severe phytotoxicity, reducing shoot fresh weight by 42.3% and root length by 55.1%.
- Oxidative stress was significantly higher in plants exposed to micro-sized MPs, with MDA content increasing by 263.4%.
- The bioaccumulation of microplastics followed a non-linear pattern and was best described by the Freundlich isotherm model (R2 > 0.97).

## Abstract

Microplastic (MP) contamination in agricultural soils poses a growing threat to crop health, yet the size-dependent mechanisms governing their uptake and phytotoxicity remain poorly understood. This study investigated the physiological and biochemical responses of tomato (Solanum lycopersicum L.) seedlings exposed to polyethylene (PE) microplastics of four distinct particle sizes at a constant mass concentration (1% w/w): T1 (1–2 mm), T2 (0.2–1 mm), T3 (50–200 μm), and T4 (1–50 μm). Results showed that PE exposure significantly inhibited plant growth in a size-dependent manner. The T4 treatment (1–50 μm) caused the most severe phytotoxicity, reducing shoot fresh weight by 42.3% and total root length by 55.1% compared to the control, indicating that micro-sized particles severely restrict root system expansion. This growth retardation was accompanied by aggravated oxidative stress, evidenced by a 263.4% surge in malondialdehyde (MDA) content (reaching 29.8 nmol/g FW) in the T4 group. To mitigate this stress, the antioxidant defense system was significantly activated, with SOD, POD, and CAT activities increasing by 122.2%, 194.1%, and 177.8%, respectively. The bioaccumulation of PE in plant tissues was highly non-linear and fitted well to the Freundlich isotherm model (R2 > 0.97). Notably, the uptake and mobility of MPs were strongly governed by particle size, as reflected by the bioconcentration factor (BCF) and translocation factor (TF). Both indices exhibited a sharp increase as particle size decreased: root BCF surged from 0.016 (T1) to 0.840 (T4), while TF rose from 0.125 to 0.286, confirming the exponentially higher bioavailability and upward translocation potential of micro-sized particles (T4). Physiologically, small-sized MPs (T3, T4) induced non-stomatal limitations to photosynthesis. Furthermore, Variance Partitioning Analysis (VPA) revealed a distinct mechanistic shift around a critical size threshold: while growth inhibition under large-sized MP exposure (T1, T2) was primarily driven by disruptions in indole-3-acetic acid (IAA) homeostasis (explaining 32.4% of variation), the toxicity of small-sized MPs was predominantly governed by oxidative stress responses (explaining 38.6% of variation). These findings highlight that environmental risk assessments based solely on mass concentration may underestimate the hazards of micro-sized fragments, which exert toxicity through fundamentally different physiological pathways compared to larger particles. Ultimately, the identified shifts in hormonal balance and oxidative status provide a valuable mechanistic framework for evaluating the potential impacts of microplastic stress on the nutritional composition and overall quality of tomato fruits in subsequent growth stages.

## Linked entities

- **Chemicals:** malondialdehyde (PubChem CID 10964), indole-3-acetic acid (PubChem CID 802)
- **Species:** Solanum lycopersicum (taxon 4081)

## Full-text entities

- **Genes:** Peroxidase [NCBI Gene 543959], Catalase [NCBI Gene 543990], FESOD (iron superoxide dismutase) [NCBI Gene 544259] {aka Fe-SODle, sodb}
- **Diseases:** nutritional deficit (MESH:D009748), Toxicity (MESH:D064420), growth retardation (MESH:D006130)
- **Chemicals:** T3 (MESH:D014284), IAA (MESH:C030737), auxin (MESH:D007210), MP (MESH:D000080545), ROS (MESH:D017382), ethanol (MESH:D000431), PE (MESH:D020959), CO2 (MESH:D002245), water (MESH:D014867), TBA (MESH:C029684), lipid (MESH:D008055), nitrogen (MESH:D009584), sodium hypochlorite (MESH:D012973), carbon (MESH:D002244), MDA (MESH:D008315), methanol (MESH:D000432), T4 (MESH:D013974), H2O2 (MESH:D006861), BCF (-), superoxide (MESH:D013481), formic acid (MESH:C030544), phosphorus (MESH:D010758)
- **Species:** Homo sapiens (human, species) [taxon 9606], Solanum lycopersicum (tomato, species) [taxon 4081]

## Full text

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## Figures

4 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12957103/full.md

## References

36 references — full list in the complete paper: https://tomesphere.com/paper/PMC12957103/full.md

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Source: https://tomesphere.com/paper/PMC12957103