Abstract
The pulmonary damage induced by nanosized titanium dioxide (nano-TiO2) is of great concern, but the mechanism of how this damage may be incurred has yet to be elucidated. Here, we examined how multiple genes may be affected by nano-TiO2 exposure to contribute to the observed damage. The results suggest that long-term exposure to nano-TiO2 led to significant increases in inflammatory cells, and levels of lactate dehydrogenase, alkaline phosphate, and total protein, and promoted production of reactive oxygen species and peroxidation of lipid, protein and DNA in mouse lung tissue. We also observed nano-TiO2 deposition in lung tissue via light and confocal Raman microscopy, which in turn led to severe pulmonary inflammation and pneumonocytic apoptosis in mice. Specifically, microarray analysis showed significant alterations in the expression of 847 genes in the nano-TiO2-exposed lung tissues. Of 521 genes with known functions, 361 were up-regulated and 160 down-regulated, which were associated with the immune/inflammatory responses, apoptosis, oxidative stress, the cell cycle, stress responses, cell proliferation, the cytoskeleton, signal transduction, and metabolic processes. Therefore, the application of nano-TiO2 should be carried out cautiously, especially in humans.
Highlights
Nanosized titanium dioxide particles, due to their high surface area to particle mass ratio, have been increasingly used as catalysts and are being commercially manufactured for use in medical, diagnostic, energy, component, and cosmetic applications as opposed to bulk TiO2 [1,2]
We investigated gene expression profiles of the murine lung to explore mechanisms of immune/inflammation responses, apoptosis, and oxidative stress induced by exposure to nano-TiO2 for 90 consecutive days to serve as a reference for future mechanistic studies on the effects of nano-TiO2 and other NPs in pulmonary toxicity to animals and humans
Black deposits were observed in the pneumonocytes exposed to 10 mg/kg of nanoTiO2 via transmission electron microscopy (TEM) (Fig. 2d) and Raman signals of nano-TiO2 were exhibited via confocal Raman microscopy (Fig. 2d)
Summary
Nanosized titanium dioxide (nano-TiO2) particles, due to their high surface area to particle mass ratio, have been increasingly used as catalysts and are being commercially manufactured for use in medical, diagnostic, energy, component, and cosmetic applications as opposed to bulk TiO2 (micrometer-sized) [1,2]. Concerns have been raised over the safety of nano-TiO2 particles, as the toxicological effects of nano-TiO2 have been demonstrated through several exposure routes, including dermal, oral, and pulmonary. Following inhalation, nano-TiO2 particles are internalized by clathrin-mediated endocytosis, caveolin-mediated endocytosis, and macropinocytosis by both phagocytic and non-phagocytic cells [3]. The pulmonary responses induced by inhaled nanoparticles (NPs) are considered to be greater than those produced by micron-sized particles because of the increased surface area to particle mass ratio [4,5]
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