Inflammatory response in human alveolar epithelial cells after TiO NPs or ZnO NPs exposure: Inhibition of surfactant protein A expression as an indicator for loss of lung function
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Final Accepted Manuscript
Author
Jiménez-Chávez, ASolorio-Rodríguez, A
Escamilla-Rivera, V
Leseman, D
Morales-Rubio, R
Uribe-Ramírez, M
Campos-Villegas, L
Medina-Ramírez, I E
Arreola-Mendoza, L
Cassee, F R
De Vizcaya-Ruiz, A
Affiliation
Departament of Otolaryngology – Head & Neck Surgery, College of Medicine, University of ArizonaIssue Date
2021-04-03
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Elsevier B.V.Citation
Jiménez-Chávez, A., Solorio-Rodríguez, A., Escamilla-Rivera, V., Leseman, D., Morales-Rubio, R., Uribe-Ramírez, M., ... & De Vizcaya-Ruiz, A. (2021). Inflammatory response in human alveolar epithelial cells after TiO2 NPs or ZnO NPs exposure: inhibition of surfactant protein A expression as an indicator for loss of lung function. Environmental Toxicology and Pharmacology, 103654.Rights
Copyright © 2021 Elsevier B.V. All rights reserved.Collection Information
This item from the UA Faculty Publications collection is made available by the University of Arizona with support from the University of Arizona Libraries. If you have questions, please contact us at repository@u.library.arizona.edu.Abstract
The increasing use of metal oxide nanoparticles (MONPs) as TiO2 NPs or ZnO NPs has led to environmental release and human exposure. The respiratory system, effects on lamellar bodies and surfactant protein A (SP-A) of pneumocytes, can be importantly affected. Exposure of human alveolar epithelial cells (A549) induced differential responses; a higher persistence of TiO2 in cell surface and uptake (measured by Atomic Force Microscopy) and sustained inflammatory response (by means of TNF-α, IL-10, and IL-6 release) and ROS generation were observed, whereas ZnO showed a modest response and low numbers in cell surface. A reduction in SP-A levels at 24 h of exposure to TiO2 NPs (concentration-dependent) or ZnO NPs (the higher concentration) was also observed, reversed by blocking the inflammatory response (by the inhibition of IL-6). Loss of SP-A represents a relevant target of MONPs-induced inflammatory response that could contribute to cellular damage and loss of lung function.Note
12 month embargo; available online 3 April 2021EISSN
1872-7077PubMed ID
33823299Version
Final accepted manuscriptae974a485f413a2113503eed53cd6c53
10.1016/j.etap.2021.103654
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