Harnessing rat derived model cells to assess the toxicity of TiO2 nanoparticles

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作者
Manizheh Sarikhani
Sevil Vaghefi Moghaddam
Masoumeh Firouzamandi
Marzie Hejazy
Bahareh Rahimi
Hassan Moeini
Effat Alizadeh
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[1] Tabriz University of Medical Sciences,Department of Medical Biotechnology, Faculty of Advanced Medical Sciences
[2] University of Tabriz,Biotechnology Section, Department of Pathobiology, Faculty of Veterinary Medicine
[3] University of Tabriz,Toxicology Section, Department of Basic Science, Faculty of Veterinary Medicine
[4] Iran University of Medical Sciences,Department of Medical Biotechnology, Faculty of Allied Medical Sciences
[5] Technische Universität of München,Institute of Virology, Faculty of Medicine
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Until now, a few studies have been conducted on the destructive effects of TiO2 NPs in living organisms, and studies on the toxicity of TiO2 NPs are still in the beginning phases. Because of the widespread use of TiO2 NPs in all areas of human life, it is essential to study their profound and fundamental toxic effects on each organ and body cell. Herein, we evaluate the effect of exposure to TiO2 NPs on in vitro models derived from the rat bone marrow and adipose tissues. Exposure to TiO2 NPs at 100 and 200 μg/ml exhibited cytotoxicity for the rat bone marrow mesenchymal stem cells (rBMSCs) and rat adipose mesenchymal stem cells (rATSC), respectively. Additionally, reduced rBMSCs and rATSCs frequencies in the S phase of the cell cycle. Moreover, TiO2 NPs enhanced the activity of cellular senescence-associated β-galactosidase in both model cells. Significantly higher relative expression of aging-related genes P53 and NF-kB (p < 0.05) and lower expression levels of anti-aging-related genes Nanog and SIRT1 were found in the treated cells (p < 0.05). Colony-forming and DAPI staining showed the reduction of cell growth and DNA damage in both rBMSCs and rATSCs. Our findings along with other similar findings showed that TiO2 NPs probably have negative effects on the cell growth, prompt the cells for entry into proliferation stop, DNA damage, and trigger the aging process.
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