Polystyrene Microplastics Postpone APAP-Induced Liver Injury through Impeding Macrophage Polarization

Jing Liu1,2,3, Lecong Zhang1, Fang Xu1,3

  • 1College of Eco-Environmental Engineering, Guizhou Minzu University, Guiyang 550025, China.

Toxics
|December 22, 2022
PubMed

Insights

Polystyrene microplastics (PS MPs) impair liver repair following acetaminophen (APAP) induced liver injury by delaying crucial macrophage polarization, increasing mortality and liver damage in mice.

Area of Science:

  • Environmental toxicology
  • Hepatology
  • Immunology

Background:

  • Polystyrene microplastics (PS MPs) are pervasive environmental contaminants found in numerous organisms.
  • Previous research indicates PS MPs can cause damage to cognitive, cardiac, intestinal, and hepatic systems.
  • The specific impact of PS MPs on liver regeneration during drug-induced liver injury (DILI) is not well understood.

Purpose of the Study:

  • To investigate the effects of PS MPs on liver repair mechanisms in a mouse model of acetaminophen (APAP)-induced liver injury.
  • To elucidate the underlying cellular and molecular mechanisms by which PS MPs influence liver regeneration.

Main Methods:

  • Mice were pretreated with PS MPs before APAP administration to induce acute liver injury.
  • Evaluated parameters included mortality, hepatocyte apoptosis, cell proliferation, and inflammatory responses.
  • Immune cell recruitment and macrophage polarization were analyzed using flow cytometry and histological assessments.

Main Results:

  • PS MPs pretreatment significantly increased mortality and hepatocyte apoptosis in APAP-induced liver injury.
  • Exposure to PS MPs suppressed hepatic cell proliferation and altered the inflammatory milieu.
  • While PS MPs recruited neutrophils and macrophages, they delayed the polarization of macrophages towards an anti-inflammatory phenotype, hindering tissue repair.

Conclusions:

  • Polystyrene microplastics exacerbate APAP-induced hepatotoxicity and impede liver regeneration.
  • Delayed macrophage polarization is identified as a key mechanism underlying PS MP-induced suppression of liver repair.
  • These findings highlight the potential health risks associated with PS MP exposure, particularly in individuals with compromised liver function, necessitating their consideration in health risk assessments.

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