2. Academic Validation
  3. Foodborne PET Microplastic Contamination Compromises Intestinal Barrier through a Mitochondrial-AMPK-DNA Damage Pathway

Foodborne PET Microplastic Contamination Compromises Intestinal Barrier through a Mitochondrial-AMPK-DNA Damage Pathway

  • J Agric Food Chem. 2026 Feb 18;74(6):5718-5730. doi: 10.1021/acs.jafc.5c15484.
Chuxin Zhang 1,  Yitao Yan 2,  Xu Li 1,  Jiaxing An 1,  Wenjing Li 3,  Juan Shao 1,  Zhongyuan Guo 1
Affiliations

Affiliations

  • 1 School of Forensic Medicine, Shanxi Medical University, Shanxi Key Laboratory of Forensic Medicine, and Key Laboratory of Forensic Toxicology, Ministry of Public Security, Jinzhong 030600, China.
  • 2 The First Clinical Medical School, Shanxi Medical University, Taiyuan 030001, China.
  • 3 Academy of Medical Sciences, Shanxi Medical University, Jinzhong 030600, China.
PMID: 41657037 DOI: 10.1021/acs.jafc.5c15484
Abstract

Poly(ethylene terephthalate) microplastics (PET-MPs), prevalent dietary contaminants, pose potential risks to intestinal health; yet underlying mechanisms of sustained exposure remain poorly defined. We evaluated the toxicity of gastrointestinal-digested PET-MPs in a human intestinal epithelial coculture model for 24 h. Digested PET-MPs triggered cytotoxicity, oxidative stress, barrier disruption, and dysregulated cytokines, impairing epithelial homeostasis. Untargeted metabolomics identified the AMPK signaling pathway as a perturbed node. Functional validation confirmed that PET-MPs induced mitochondrial damage, resulting in ATP depletion and AMPK activation. This persistent activation mediated cellular proliferation arrest and DNA double-strand breaks. Critically, pharmacological inhibition of AMPK alleviated barrier defects and DNA damage. These results unveil a mitochondrial dysfunction-AMPK activation-DNA damage axis as a central mechanism in PET-MP-induced injury, providing mechanistic insight into the health risks of microplastic exposure.

Keywords

AMPK signaling; DNA damage; PET microplastics; intestinal barrier dysfunction; mitochondrial dysfunction.

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