4.7 Article

Functionalized Titanium Nanoparticles Induce Oxidative Stress and Cell Death in Human Skin Cells

Journal

INTERNATIONAL JOURNAL OF NANOMEDICINE
Volume 17, Issue -, Pages 1495-1509

Publisher

DOVE MEDICAL PRESS LTD
DOI: 10.2147/IJN.S325767

Keywords

nanoparticle; titanium; cytotoxicity; human skin cells

Funding

  1. PETROBRAS
  2. Biophotonics Laboratory from SAo Carlos Institute of Physics, University of SAo Paulo

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This study evaluated the cytotoxicity of a new titanium nanoparticle functionalized with a sodium carboxylic ligand in human keratinocytes and human fibroblasts. The results demonstrated decreased cell viability at the highest concentrations tested for both cell lines, with only fibroblasts showing cell membrane damage and increased reactive oxygen species production. The study suggests that the cytotoxicity mechanism is dependent on cell type, dose, and time.
Purpose: Nanoparticles are resources of advanced nanotechnology being present in several products. Titanium dioxide nanoparticles are among the five most widely used NP currently expanding their benefits from the oil industry to the areas of diagnostic medicine due to their properties and small size. However, its impact on human health is still controversial in the literature. We aimed to evaluate the cytotoxicity of a new titanium NP functionalized with sodium carboxylic ligand (COOH-Na+) in human keratinocytes (HaCaT) and human fibroblasts (HDFn). Methods: The physical-chemical characterization was performed by the transmission electron microscopy (TEM), dynamic light scattering (DLS) and zeta potential techniques, respectively. MTT and LDH assays were used to assess cytotoxicity and cell membrane damage respectively, ELISA to identify the inflammatory profile and, reactive oxygen species assay and cytometry to detect reactive oxygen species and their relationship with apoptosis/necrosis mechanisms. Results: The results demonstrated a decrease in cell viability at the highest concentrations tested for both cell lines, but no change in LDH release was detected for the HaCaT. The cell membrane damage was found only at 100.0 mu g/mL for the HDFn. It was demonstrated that cytotoxicity in the highest concentrations evaluated for both cell lines for the 72 h period. The HDFn showed damage to the cell membrane at a concentration of 100 mu g/mL followed by a significant increase in reactive oxygen species production. No inflammatory profile was detected. The HaCaT showed apoptosis when exposed to the highest concentration evaluated and HDFn showed both apoptosis and necrosis for the same concentration. Conclusion: Thus, it is possible to conclude that the cytotoxicity mechanism differs according to the cell type evaluated, with HDFn being the most sensitive line in this case, and this mechanism can be defined in a dose and time dependent manner, since the highest concentrations also triggered death cell.

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