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Nanoceria’s Silent Threat: Investigating Acute and Sub-Chronic Effects of CeO2 Nanopowder (≤50 nm) on the Human Intestinal Epithelial Cells

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A. Laganà, A. Laganà, A. Laganà, Alessio Facciolà, A. Laganà, A. Laganà, Alessio Facciolà, A. Laganà, Pietro Picerno, Alessio Facciolà, Caterina Saija, Alessio Facciolà, Alessio Facciolà, Alessio Facciolà, Maria Paola Bertuccio, Caterina Saija, Alessio Facciolà, Alessio Facciolà, Alessio Facciolà, Maria Paola Bertuccio, Giuseppa Visalli, A. Laganà, Giuseppa Visalli Giuseppa Visalli

Summary

Researchers investigated the effects of cerium dioxide nanoparticles on human intestinal cells over both short-term and extended exposure periods up to 35 days. The study found that while cells could initially recover from mitochondrial damage through protective autophagy pathways, prolonged sub-chronic exposure led to irreversible cell damage, including DNA repair saturation and increased cell death.

Study Type In vitro

The increased mobilization of Rare Earth Elements (REEs), due to emerging technologies, could impact human health. The study assessed the effects of CeO<sub>2</sub> nanopowder (100 μg/mL) in human intestinal cells (HT-29) following both acute (24 h) and, a novelty for in vitro study, sub-chronic exposure, treating subcultures of exposed cells to CeO<sub>2</sub> NP up to 35 days. Recovery was also examined in exposed cells' progeny. CeO<sub>2</sub> NP internalization and acute cytotoxicity were dose and time dependent. A significant pro-oxidant effect was observed for up to 14 days. The highest mitochondrial impairment was detected after 7 days, but in post-exposure experiments the recovery was observed. Conversely, genotoxicity highlighted the saturation of the DNA repair mechanisms. The irreversible cell damage of sub-chronic exposure was highlighted by the percentage of death cells (<i>p</i> = 0.011) and by the weekly cell replication index (5.68 vs. 7.41). The homeostatic mitophagy pathway was able to counteract ROS-induced mitochondrial dysfunction, as shown by overexpression of ATG5, LC3, and BECN1 genes throughout the examined times. Instead, the overexpression of the pro-apoptotic gene Bax was very brief, highlighting that prolonged exposure might cause more widespread adverse effects, also involving cells that are not directly exposed to nanoceria.

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