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Molecular mechanisms of nanosized titanium dioxide-induced pulmonary injury in mice
Bing Li1, Yuguan Ze, Qingqing Sun
1Medical College of Soochow University, Suzhou, China.
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.
Insights
Long-term exposure to nanosized titanium dioxide (nano-TiO2) causes lung damage by increasing inflammation, oxidative stress, and altering gene expression. Caution is advised for nano-TiO2 applications, particularly in humans.
Area of Science:
- Toxicology
- Nanotechnology
- Molecular Biology
Background:
- Pulmonary damage from nanosized titanium dioxide (nano-TiO2) is a concern.
- The precise mechanisms underlying nano-TiO2-induced lung injury remain unclear.
Purpose of the Study:
- To investigate the molecular mechanisms of pulmonary damage induced by nano-TiO2 exposure.
- To identify specific genes and pathways affected by nano-TiO2 in lung tissue.
Main Methods:
- Exposure of mice to nano-TiO2.
- Biochemical assays for inflammatory markers and oxidative stress.
- Light and confocal Raman microscopy for nano-TiO2 deposition.
- Microarray analysis to assess gene expression changes.
Main Results:
- Nano-TiO2 exposure increased inflammatory cells, lactate dehydrogenase, alkaline phosphatase, and total protein.
- Increased reactive oxygen species and lipid, protein, and DNA peroxidation were observed.
- Significant alterations in 847 genes, including those related to immune response, apoptosis, and oxidative stress, were identified.
- Nano-TiO2 deposition in lung tissue correlated with inflammation and apoptosis.
Conclusions:
- Nano-TiO2 exposure induces significant pulmonary inflammation, oxidative stress, and apoptosis.
- Altered gene expression profiles provide insights into the molecular pathogenesis of nano-TiO2 lung injury.
- Cautious application of nano-TiO2 is recommended due to potential risks to human health.
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