Effects of true-to-life PET nanoplastics using primary human nasal epithelial cells

Since inhalation is a relevant exposure route, studies using appropriate micro/nanoplastic (MNPLs) models, representative targeted cells, and relevant biomarkers of effect are required. We have used lab-made polyethylene terephthalate (PET)NPLs obtained from PET plastic water bottles. Human primary...

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Veröffentlicht in:Environmental toxicology and pharmacology 2023-06, Vol.100, p.104140-104140, Article 104140
Hauptverfasser: Annangi, Balasubramanyam, Villacorta, Aliro, Vela, Lourdes, Tavakolpournegari, Alireza, Marcos, Ricard, Hernández, Alba
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Sprache:eng
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Zusammenfassung:Since inhalation is a relevant exposure route, studies using appropriate micro/nanoplastic (MNPLs) models, representative targeted cells, and relevant biomarkers of effect are required. We have used lab-made polyethylene terephthalate (PET)NPLs obtained from PET plastic water bottles. Human primary nasal epithelial cells (HNEpCs) were used as a model of the first barrier of the respiratory system. Cell internalization and intracellular reactive oxygen species (iROS) induction, as well as the effects on mitochondria functionality and in the modulation of the autophagy pathway, were evaluated. The data indicated significant cellular uptake and increased levels of iROS. Furthermore, a loss of mitochondrial membrane potential was observed in the exposed cells. Regarding the effects on the autophagy pathway, PETNPLs exposure significantly increases LC3-II protein expression levels. PETNPLs exposure also induced significant increases in the expression of p62. This is the first study showing that true-to-life PETNPLs can alter the autophagy pathway in HNEpCs. [Display omitted] •True-to-life PET nanoplastics were evaluated for hazard assessment.•Primary human nasal epithelial cells were used as a target of inhalation exposure.•Cell internalization and intracellular ROS induction were demonstrated.•PETNPLs exposure induced mitochondrial membrane potential loss.•Changes in the autophagy pathway, as a mechanism maintaining cellular homeostasis, were induced.
ISSN:1382-6689
1872-7077
DOI:10.1016/j.etap.2023.104140