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In Vitro and In Vivo Approaches to Determine Intestinal Epithelial Cell Permeability
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Air Pollution Quinones Impair Intestinal Barrier Integrity and Endoplasmic Reticulum in Differentiated Caco-2 Cells.

Franco Cervellati1, Giulia Trinchera2, Alice Casoni2

  • 1Department of Neuroscience and Rehabilitation, University of Ferrara, Ferrara, Italy.

Journal of Applied Toxicology : JAT
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PubMed
Summary

Air pollution components, specifically redox-active quinones, damage intestinal barrier integrity. This damage is linked to oxidative stress, endoplasmic reticulum stress, and altered cell junctions in the gut.

Keywords:
intercellular junctionsintestinal barrierorganic pollutantsoxinflammationquinones

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Published on: May 13, 2020

Area of Science:

  • Environmental Health
  • Toxicology
  • Gastroenterology

Background:

  • Particulate matter (PM) poses a global health risk, with components entering the gastrointestinal tract.
  • Redox-active quinones within PM are implicated in toxicity, but their impact on intestinal epithelial integrity is not fully understood.

Purpose of the Study:

  • To investigate the effects of 1,2-naphthoquinone (NQ) and 9,10-phenanthrenequinone (PQ) on human intestinal epithelial cells.
  • To assess the role of oxidative stress, endoplasmic reticulum (ER) stress, and junctional protein alterations in quinone-induced barrier dysfunction.

Main Methods:

  • Human Caco-2 cells were exposed to NQ and PQ.
  • Assessed oxidative potential, intracellular ROS, ER stress markers (GRP78, IRE1, ATF6), pro-inflammatory cytokines (IL-1α, IL-6, TNFα).
  • Evaluated ultrastructural changes, junctional protein expression (Connexin-43, E-cadherin), and barrier function (TEER).

Main Results:

  • Quinone exposure induced intracellular ROS and upregulated ER stress and pro-inflammatory cytokine genes.
  • Ultrastructural analysis revealed ER dilation and altered intercellular junctions.
  • Combined quinone exposure significantly reduced transepithelial electrical resistance (TEER) and decreased junctional protein expression.

Conclusions:

  • Redox-active quinones impair intestinal barrier integrity in differentiated epithelial models.
  • Oxidative stress, ER stress activation, and junctional protein alterations are key mechanisms involved.
  • The mature intestinal barrier is vulnerable to specific PM constituents, with ER stress pathways playing a role in pollutant-induced dysfunction.