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The iron matters: Aged microplastics disrupted the iron homeostasis in the liver organoids

Wei Cheng1, Yue Zhou1, Hange Chen1

  • 1School of Public Health, Shanghai Jiao Tong University School of Medicine, Shanghai, China.

The Science of the Total Environment
|October 3, 2023
PubMed

Insights

Aged microplastics (aMP) show greater liver toxicity than pristine microplastics (pMP). Aged polystyrene microplastics disrupt iron homeostasis and mitochondrial function in liver organoids, highlighting potential health risks from microplastic exposure.

Area of Science:

  • Environmental Toxicology
  • Cell Biology
  • Materials Science

Background:

  • Plastic products degrade into aged microplastics (aMP) through daily use.
  • Humans are exposed to aMP, with the liver being a critical target organ.
  • Limited research compares the hepatic toxicity of aMP versus pristine microplastics (pMP).

Purpose of the Study:

  • To compare the cytotoxicity of aged polystyrene microplastics (aPS) and pristine polystyrene microplastics (pPS) in human liver organoids (LOs).
  • To investigate the impact of aPS exposure on iron homeostasis, mitochondrial function, and oxidative stress in LOs.
  • To explore potential protective effects of N-acetylcysteine (NAC) and exacerbating effects of iron overload (ferric ammonium citrate - FAC) on aPS-induced liver toxicity.

Main Methods:

  • Cultured human pluripotent stem cells-derived liver organoids (LOs).
  • Exposed LOs to varying concentrations of pPS and aPS (1 μm).
  • Analyzed cytotoxicity, iron levels ([Fe2+], [Fe3+]), iron transport markers (TFRC, SLC7A11, FTL, FTH1), mitochondrial morphology, lipid peroxidation, and GSH peroxidase activity.
  • Utilized FAC for iron overload and NAC for oxidative stress modulation.

Main Results:

  • aPS exhibited higher cytotoxicity than pPS in LOs.
  • aPS exposure disrupted iron homeostasis, indicated by altered iron levels and co-localization with ferritin light chain (FTL), suggesting a "vector-like effect".
  • Observed abnormal mitochondrial morphology, increased lipid peroxidation, decreased GSH peroxidase activity, and altered expression of iron-related genes (TFRC, SLC7A11, FTL, FTH1).
  • Iron overload exacerbated aPS toxicity, while NAC partially mitigated oxidative stress but did not fully reverse hepatotoxicity.
  • Low-dose aMP (50 ng/mL) induced a specific dimorphic change in FTL and FTH1 expression.

Conclusions:

  • Aged microplastics pose a greater hepatic risk than pristine microplastics.
  • aPS-induced liver toxicity involves the disruption of iron homeostasis and mitochondrial dysfunction.
  • Further research is needed to understand the long-term health implications of aMP exposure and its specific mechanisms in the liver.
Keywords:
Aged microplasticsAlternative testGPX4HepatocytotoxicityIron homeostasisMDA

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