Polystyrene microplastics induces the injury of human corneal epithelial cells through ROS-mediated p53 pathway

Jianfeng Long1, Limin Deng1, Jian Liu1

  • 1Department of Clinical Nutrition, the 2nd Xiangya Hospital of Central South University, Changsha, 410011, China.

Mutagenesis
|June 12, 2025
PubMed
Abstract

Insights

Polystyrene microplastics (PS-MPs) harm human corneal cells by causing DNA damage and cell death, linked to oxidative stress. Antioxidants can mitigate these toxic effects, suggesting a protective mechanism against microplastic-induced cellular damage.

Area of Science:

  • Ocular toxicology
  • Environmental health
  • Cell biology

Background:

  • Microplastic pollution is a growing environmental concern.
  • The impact of microplastics on ocular tissues is not well understood.
  • Human corneal epithelial cells (HCEP) are the first line of defense against external factors in the eye.

Purpose of the Study:

  • To investigate the toxicological effects of polystyrene microplastics (PS-MPs) on human corneal epithelial cells (HCEP).
  • To elucidate the underlying mechanisms of PS-MP-induced cellular damage in HCEP.

Main Methods:

  • Cytotoxicity was assessed using CCK-8 assays.
  • Cell cycle, apoptosis, and necrosis were analyzed by flow cytometry.
  • Reactive oxygen species (ROS) and DNA damage (γ-H2AX) were detected via immunofluorescence.
  • Protein expression related to cell death pathways was evaluated using western blotting.

Main Results:

  • PS-MP cytotoxicity was dependent on particle size and concentration, with smaller particles and higher concentrations causing more harm.
  • Exposure to PS-MPs induced cell cycle arrest, necrosis, and apoptosis in HCEP cells.
  • PS-MPs led to excessive ROS production and DNA damage, which were mitigated by ROS scavengers.
  • ROS scavengers reversed PS-MP-induced alterations in key proteins involved in cell cycle regulation, necrosis, and apoptosis.

Conclusions:

  • PS-MP exposure induces significant cellular damage in HCEP, including cell cycle arrest, necrosis, and apoptosis.
  • This damage is mediated by ROS overproduction and subsequent activation of the P53 signaling pathway.
  • The findings highlight the potential ocular toxicity of microplastics and suggest ROS-related pathways as therapeutic targets.

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