Genotoxic and inflammatory effects of nanofibrillated cellulose in murine lungs
| Autor: | Elina Rydman, Denilson Da Silva Perez, Henrik Wolff, Julia Catalán, Martin Willemoës, Ulla Forsström, Casper Højgaard, Kukka Aimonen, Asko Sneck, Kai Savolainen, Ulla Vogel, Jacob R. Winther, Harri Alenius, Kati-Susanna Hannukainen, Satu Suhonen, Valérie Meyer, Carlos Moreno, Hannu Norppa, Esa Vanhala |
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| Rok vydání: | 2016 |
| Předmět: |
0301 basic medicine
Pathology Erythrocytes Health Toxicology and Mutagenesis medicine.medical_treatment NFC Nanofibers 02 engineering and technology Toxicology medicine.disease_cause Mice Lung nanocellulose lungs Genetics (clinical) Micronucleus Tests medicine.diagnostic_test Chemistry cellulose nanofibrils respiratory system 021001 nanoscience & nanotechnology medicine.anatomical_structure Cytokine Micronucleus test Cytokines Female Comet Assay medicine.symptom 0210 nano-technology safety medicine.medical_specialty mice ta221 ta1172 Bone Marrow Cells Inflammation 03 medical and health sciences Genetics medicine Animals SDG 7 - Affordable and Clean Energy Cellulose mouse Micronuclei Chromosome-Defective ta1184 Macrophages genotoxicity ta1182 occupational safety DNA Comet assay 030104 developmental biology Bronchoalveolar lavage inflammation Immunology DNA damage Bone marrow nanofibrillated cellulose Genotoxicity DNA Damage |
| Zdroj: | Europe PubMed Central Catalán, J, Rydman, E, Aimonen, K, Hannukainen, K-S, Suhonen, S, Vanhala, E, Moreno, C, Meyer, V, da Silva Perez, D, Sneck, A, Forsström, U, Højgaard, C, Willemoes, M, Winther, J R, Vogel, U, Wolff, H, Alenius, H, Savolainen, K M & Norppa, H 2017, ' Genotoxic and inflammatory effects of nanofibrillated cellulose in murine lungs ', Mutagenesis, vol. 32, no. 1, pp. 23-31 . https://doi.org/10.1093/mutage/gew035 Zaguán. Repositorio Digital de la Universidad de Zaragoza instname |
| ISSN: | 1464-3804 0267-8357 |
| Popis: | Nanofibrillated cellulose (NFC) is a sustainable and renewable nanomaterial, with diverse potential applications in the paper and medical industries. As NFC consists of long fibres of high aspect ratio, we examined here whether TEMPO-(2, 2, 6, 6-tetramethyl-piperidin-1-oxyl) oxidised NFC (length 300-1000 nm, thickness 10-25 nm), administrated by a single pharyngeal aspiration, could be genotoxic to mice, locally in the lungs or systemically in the bone marrow. Female C57Bl/6 mice were treated with four different doses of NFC (10, 40, 80 and 200 mu g/mouse), and samples were collected 24 h later. DNA damage was assessed by the comet assay in bronchoalveolar lavage (BAL) and lung cells, and chromosome damage by the bone marrow erythrocyte micronucleus assay. Inflammation was evaluated by BAL cell counts and analysis of cytokines and histopathological alterations in the lungs. A significant induction of DNA damage was observed at the two lower doses of NFC in lung cells, whereas no increase was seen in BAL cells. No effect was detected in the bone marrow micronucleus assay, either. NFC increased the recruitment of inflammatory cells to the lungs, together with a dose-dependent increase in mRNA expression of tumour necrosis factor a, interleukins 1 beta and 6, and chemokine (C-X-C motif) ligand 5, although there was no effect on the levels of the respective proteins. The histological analysis showed a dose-related accumulation of NFC in the bronchi, the alveoli and some in the cytoplasm of macrophages. In addition, neutrophilic accumulation in the alveolar lung space was observed with increasing dose. Our findings showed that NFC administered by pharyngeal aspiration caused an acute inflammatory response and DNA damage in the lungs, but no systemic genotoxic effect in the bone marrow. The present experimental design did not, however, allow us to determine whether the responses were transient or could persist for a longer time. |
| Databáze: | OpenAIRE |
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