Kazan (Volga region) Federal University, KFU
KAZAN
FEDERAL UNIVERSITY
 
MECHANISMS RELATED TO CARBON NANOTUBES GENOTOXICITY IN HUMAN CELL LINES OF RESPIRATORY ORIGIN
Form of presentationArticles in international journals and collections
Year of publication2024
Языкрусский
  • Daminova Amina Galeevna, author
  • Minibaeva Farida Vilevna, author
  • Bibliographic description in the original language Fatkhutdinova L. M. Mechanisms related to carbon nanotubes genotoxicity in human cell lines of respiratory origin / L. M. Fatkhutdinova, G. F. Gabidinova, A. G. Daminova, A. M. Dimiev, T. L. Khamidullin, E. V. Valeeva, A. E. E. Cokou, S. Z. Validov, G. A. Timerbulatova // Toxicology and Applied Pharmacology. - 2024. - V. 482. - № 116784. - P. 1-16.
    Annotation Potential genotoxicity and carcinogenicity of carbon nanotubes (CNT), as well as the underlying mechanisms, remains a pressing topic. The study aimed to evaluate and compare the genotoxic effect and mechanisms of DNA damage under exposure to different types of CNT. μ Immortalized human cell lines of respiratory origin BEAS-2B, A549, MRC5-SV40 were exposed to three types of CNT: MWCNT Taunit-M, pristine and purified SWCNT TUBALL? at concentrations in the range of 0.0006–200 g/ml. Data on the CNT content in the workplace air were used to calculate the lower concentration limit. The genotoxic potential of CNTs was investigated at non-cytotoxic concentrations using a DNA comet assay. We explored reactive oxygen species (ROS) formation, direct genetic material damage, and expression of a profibrotic factor TGFB1 as mechanisms related to genotoxicity upon CNT exposure. An increase in the number of unstable DNA regions was observed at a subtoxic concentration of CNT (20 μ g/ ml), with no genotoxic effects at concentrations corresponding to industrial exposures being found. While the three test articles of CNTs exhibited comparable genotoxic potential, their mechanisms appeared to differ. MWCNTs were found to penetrate the nucleus of respiratory cells, potentially interacting directly with genetic material, as well as to enhance ROS production and TGFB1 gene expression. For A549 and MRC5-SV40, genotoxicity depended mainly on MWCNT concentration, while for BEAS-2B – on ROS production. Mechanisms of SWCNT genotoxicity were not so obvious. Oxidative stress and increased expression of profibrotic factors could not fully explain DNA damage under SWCNT exposure, and other mechanisms might be involved.
    Keywords Carbon nanotubes, Human cell lines of respiratory origin, DNA comet assay, Nuclear translocation, Oxidative stress, Transmission electron microscopy
    The name of the journal Toxicology and Applied Pharmacology
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