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Mitochondrial Complex I hyperactivation drives PET microplastic-induced intestinal bioenergetic collapse.

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Area of Science:

  • Environmental Science
  • Toxicology
  • Biochemistry

Background:

  • Polyethylene terephthalate (PET) microplastics (MPs) are widespread environmental pollutants with known human exposure pathways.
  • Ingested MPs can cross the intestinal barrier, enter circulation, and accumulate in organs, posing potential health risks.

Purpose of the Study:

  • To investigate the effects of digestive transformation on PET MPs.
  • To elucidate the mechanisms by which digested PET MPs induce intestinal dysfunction and metabolic toxicity.

Main Methods:

  • Utilized physiologically relevant PET MPs from commercial bottles and a simulated gastrointestinal tract.
  • Employed high-resolution respirometry and integrated multi-omics profiling.
  • Assessed effects on glucose transport (GLUT2), glycolysis, mitochondrial respiration, oxidative stress markers (ROS, lipid peroxidation), and ATP synthesis.

Main Results:

  • Digested PET MPs inhibit GLUT2, causing glucose accumulation and glycolytic blockade.
  • Mitochondrial Complex I shows dysfunctional hyperactivation, leading to increased ROS generation and ATP synthesis shutdown.
  • Significant oxidative stress, lipid peroxidation, and impaired mitochondrial bioenergetics were observed, indicating a metabolic collapse.

Conclusions:

  • Digestively transformed PET MPs act as potent drivers of metabolic toxicity.
  • A novel toxic mechanism involving mitochondrial dysfunction and oxidative stress was identified.
  • Findings provide a mechanistic framework for assessing health risks associated with dietary microplastic exposure.