Titanium dioxide nanoparticles and the oral uptake-route

2013 ◽  
Vol 14 (1-2) ◽  
pp. 25-35 ◽  
Author(s):  
Eleonore Fröhlich ◽  
Birgit Johanna Teubl ◽  
Eva Roblegg
Keyword(s):  
Titanium Dioxide ◽  
Risk Evaluation ◽  
Titanium Dioxide Nanoparticles ◽  
Consumer Products ◽  
Cell Entry ◽  
Mucus Layer ◽  
Food Sector ◽  
Pharmaceutical Dosage Forms ◽  
Oral Uptake ◽  
Human Risk

AbstractTitanium dioxide (TiO2) is a common additive that is increasingly used in consumer products, food, pharmaceutical dosage forms and cosmetic articles. However, due to size reduction of TiO2 particles from the microscale to the nanoscale, application areas of this material are expanding, especially in the food sector, which makes investigations of nano-TiO2 crucial. This review focuses on two important topics of current research regarding the oral pathway: 1) anatomy of the orogastrointestinal tract, composition of epithelial and mucus layer, and pH changes; 2) cell entry mechanisms, cytotoxicity and translocation. Sufficient knowledge on the oral uptake route is not yet available but is highly needed for human risk evaluation.

scholarly journals Titanium dioxide nanoparticles exacerbate allergic airway inflammation via TXNIP upregulation in a mouse model of asthma

2021 ◽  
Author(s):  
Je-Oh Lim ◽  
Se-Jin Lee ◽  
Woong-Il Kim ◽  
So-Won Pak ◽  
Changjong Moon ◽  
...  
Keyword(s):  
Titanium Dioxide ◽  
Epithelial Cells ◽  
Mouse Model ◽  
Inflammatory Mediators ◽  
Titanium Dioxide Nanoparticles ◽  
B Cell Lymphoma ◽  
Airway Epithelial Cells ◽  
Consumer Products ◽  
Airway Epithelial ◽  
Apoptosis Pathway

Abstract Background Titanium dioxide nanoparticles (TiO2NPs) are widely used in the fields of industry and medicine and in various consumer products. With the increasing use of TiO2NPs, there has been an increase in the number of toxicity studies; however, studies investigating the mechanism underlying its toxicity are very rare. In this study, we evaluated the potential toxic effects of TiO2NPs exposure on the lungs as well as the development of asthma in ovalbumin (OVA)-induced mouse model of asthma. We also investigated the related toxic mechanism. Results TiO2NPs caused pulmonary toxicity by exacerbating the inflammatory response, indicated by an increase in the number of inflammatory cells and levels of inflammatory mediators. Exposure of mice with OVA-induced asthma to TiO2NPs led to significant increases in inflammatory mediators, cytokines, and airway hyperresponsiveness compared with non-exposed mice with asthma. This was also accompanied by an increase in inflammatory cell infiltration and mucus production in the lung tissues. TiO2NPs also decreased the expression of B-cell lymphoma 2 (Bcl2) and increased the expression of thioredoxin-interacting protein (TXNIP), phospho-apoptosis signal-regulating kinase 1, Bcl2-associated X, and cleaved-caspase 3 in the lungs of asthmatic mice compared with those of non-exposed asthmatic mice. These responses were consistent with in vitro results obtained using human airway epithelial cells. TiO2NPs treated cells exhibited an increase in the mRNA and protein expression of IL-1β, IL-6, and TNF-α with an elevation of TXNIP signaling compared to non-treated cells. Moreover, pathophysiological changes induced by TiO2NPs treatment were significantly decreased by TXNIP knockdown in the airway epithelial cells. Conclusion Taken together, TiO2NPs exposure induced toxicological changes in the respiratory tract and exacerbated the development of asthma via activation of the TXNIP-apoptosis pathway. These results provide insights into the mechanism underlying TiO2NPs-mediated respiratory toxicity.

scholarly journals Optimization of the procedure for efficient dispersion of titanium dioxide nanoparticles in aqueous samples

2016 ◽  
Vol 8 (5) ◽  
pp. 1194-1201 ◽  
Author(s):  
Janja Vidmar ◽  
Radmila Milačič ◽  
Viviana Golja ◽  
Saša Novak ◽  
Janez Ščančar
Keyword(s):  
Titanium Dioxide ◽  
Titanium Dioxide Nanoparticles ◽  
Consumer Products ◽  
Aqueous Samples

The widespread use of titanium dioxide nanoparticles (TiO2NPs) in consumer products has led to an increase of their concentrations in the environment.

Interaction of titanium dioxide nanoparticles with kaolinite clay particles in the presence of quartz sand

2020 ◽  
Author(s):  
Constantinos V. Chrysikopoulos ◽  
Dimitra Fasouletou
Keyword(s):  
Titanium Dioxide ◽  
Ionic Strength ◽  
Titanium Dioxide Nanoparticles ◽  
Rapid Development ◽  
Consumer Products ◽  
Engineered Nanoparticles ◽  
Kaolinite Clay ◽  
Clay Particles ◽  
Water Saturated ◽  
Experimental And Theoretical Studies

<p>Titanium dioxide (TiO<sub>2</sub>) is one of the most frequently employed nanoparticles (NPs) in consumer products. The rapid development of nanotechnology has led to the inevitable introduction of NPs in the natural environment, which subsequently may reach underground formations. Also, kaolinite is one of the most common minerals, which can be found in the subsurface. Numerous experimental and theoretical studies have shown that kaolinite clay particles can impact on the transport behavior of colloids, biocolloids (bacteria, viruses) and engineered nanoparticles. Therefore, the aim of this study is to examine the interaction of kaolinite (KGa-1b) particles with suspended TiO<sub>2 </sub>NPs in the presence of quartz sand.Static and dynamic batch experiments were performed with three different TiO<sub>2 </sub>concentrations (50, 100, 200 mg/L) and four different ionic strength values ​​(1, 25, 50, 100 mM). All of the experiments were conducted at room temperature (22 °C) and pH=7.The experimental results clearly suggested that TiO<sub>2 </sub>attachment onto KGa-1b particles was slightly enhanced with increasing TiO<sub>2 </sub>concentrations,but significantly increased with increasing ionic strength. Consequently, the presence of suspended KGa-1b particles can retard the TiO<sub>2 </sub>transport in water saturated porous media.</p>

Titanium dioxide nanoparticles and the oral uptake-route

nano Online ◽  
2016 ◽  
Author(s):  
Eleonore Fröhlich ◽  
Birgit Johanna Teubl ◽  
Eva Roblegg
Keyword(s):  
Titanium Dioxide ◽  
Titanium Dioxide Nanoparticles ◽  
Oral Uptake

scholarly journals Titanium Dioxide Nanoparticles Exacerbate Allergic Airway Inflammation via TXNIP Upregulation in a Mouse Model of Asthma

2021 ◽  
Vol 22 (18) ◽  
pp. 9924
Author(s):  
Je-Oh Lim ◽  
Se-Jin Lee ◽  
Woong-Il Kim ◽  
So-Won Pak ◽  
Changjong Moon ◽  
...  
Keyword(s):  
Titanium Dioxide ◽  
Epithelial Cells ◽  
Mouse Model ◽  
Titanium Dioxide Nanoparticles ◽  
B Cell Lymphoma ◽  
Airway Epithelial Cells ◽  
Consumer Products ◽  
Airway Epithelial ◽  
Mucus Production ◽  
Apoptosis Pathway

Titanium dioxide nanoparticles (TiO2NPs) are widely used in industrial and medicinal fields and in various consumer products, and their increasing use has led to an increase in the number of toxicity studies; however, studies investigating the underlying toxicity mechanism have been rare. In this study, we evaluated potential toxic effects of TiO2NPs exposure on lungs as well as the development of asthma through the ovalbumin (OVA)-induced mouse model of asthma. Furthermore, we also investigated the associated toxic mechanism. TiO2NPs caused pulmonary toxicity by exacerbating the inflammatory response, indicated by an increase in the number and level of inflammatory cells and mediators, respectively. OVA-induced asthma exposed mice to TiO2NPs led to significant increases in inflammatory mediators, cytokines, and airway hyperresponsiveness compared with those in non-exposed asthmatic mice. This was also accompanied by increased inflammatory cell infiltration and mucus production in the lung tissues. Additionally, TiO2NPs decreased the expression of B-cell lymphoma 2 (Bcl2) and the expressions of thioredoxin-interacting protein (TXNIP), phospho-apoptosis signal-regulating kinase 1, Bcl2-associated X, and cleaved-caspase 3 were escalated in the lungs of asthmatic mice compared with those in non-exposed asthmatic mice. These responses were consistent with in vitro results obtained using human airway epithelial cells. TiO2NPs treated cells exhibited an increase in the mRNA and protein expression of interleukin (IL)-1β, IL-6, and tumor necrosis factor-α with an elevation of TXNIP signaling compared to non-treated cells. Moreover, pathophysiological changes induced by TiO2NP treatment were significantly decreased by TXNIP knockdown in airway epithelial cells. Overall, TiO2NP exposure induced toxicological changes in the respiratory tract and exacerbated the development of asthma via activation of the TXNIP-apoptosis pathway. These results provide insights into the underlying mechanism of TiO2NP-mediated respiratory toxicity.

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