Concentration Dependent Toxicity of ∼20 nm Anatase Titanium Dioxide Nanoparticles—An In Vivo Study on Wistar Rats

2011 ◽  
Vol 7 (1) ◽  
pp. 207-208 ◽  
Author(s):  
Jyotisree Unnithan ◽  
MuneebU. Rehman ◽  
FarhanJ. Ahmad ◽  
M. Samim
Keyword(s):  
Titanium Dioxide ◽  
Wistar Rats ◽  
Titanium Dioxide Nanoparticles ◽  
In Vivo Study ◽  
20 Nm

scholarly journals Unraveling the neurotoxicity of titanium dioxide nanoparticles: focusing on molecular mechanisms

2016 ◽  
Vol 7 ◽  
pp. 645-654 ◽  
Author(s):  
Bin Song ◽  
Yanli Zhang ◽  
Jia Liu ◽  
Xiaoli Feng ◽  
Ting Zhou ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Titanium Dioxide ◽  
Molecular Mechanisms ◽  
Titanium Dioxide Nanoparticles ◽  
Brain Dysfunction ◽  
In Vivo Studies ◽  
Cell Components ◽  
New Perspective ◽  
The Brain

Titanium dioxide nanoparticles (TiO2 NPs) possess unique characteristics and are widely used in many fields. Numerous in vivo studies, exposing experimental animals to these NPs through systematic administration, have suggested that TiO2 NPs can accumulate in the brain and induce brain dysfunction. Nevertheless, the exact mechanisms underlying the neurotoxicity of TiO2 NPs remain unclear. However, we have concluded from previous studies that these mechanisms mainly consist of oxidative stress (OS), apoptosis, inflammatory response, genotoxicity, and direct impairment of cell components. Meanwhile, other factors such as disturbed distributions of trace elements, disrupted signaling pathways, dysregulated neurotransmitters and synaptic plasticity have also been shown to contribute to neurotoxicity of TiO2 NPs. Recently, studies on autophagy and DNA methylation have shed some light on possible mechanisms of nanotoxicity. Therefore, we offer a new perspective that autophagy and DNA methylation could contribute to neurotoxicity of TiO2 NPs. Undoubtedly, more studies are needed to test this idea in the future. In short, to fully understand the health threats posed by TiO2 NPs and to improve the bio-safety of TiO2 NPs-based products, the neurotoxicity of TiO2 NPs must be investigated comprehensively through studying every possible molecular mechanism.

scholarly journals Quercetin and Idebenone Ameliorate Oxidative Stress, Inflammation, DNA damage, and Apoptosis Induced by Titanium Dioxide Nanoparticles in Rat Liver

Dose-Response ◽  
2018 ◽  
Vol 16 (4) ◽  
pp. 155932581881218 ◽  
Author(s):  
Laila M. Fadda ◽  
Hanan Hagar ◽  
Azza M. Mohamed ◽  
Hanaa M. Ali
Keyword(s):  
Titanium Dioxide ◽  
Histopathological Examination ◽  
Titanium Dioxide Nanoparticles ◽  
Reactive Protein ◽  
Wide Range ◽  
Factor Α ◽  
Immunoglobin G ◽  
Endothelial Growth Factor

Titanium dioxide nanoparticles (TiO2-NPs) are extensively used in a wide range of applications; however, many reports have investigated their nanotoxicological effect at the molecular level either in vitro or in vivo systems. The defensive roles of quercetin (Qur) or idebenone (Id) against the hepatotoxicity induced by TiO2-NPs were evaluated in the current study. The results showed that the coadministration of Qur or Id to rats intoxicated with TiO2-NPs markedly ameliorated the elevation in hepatic malondialdehyde (MDA), serum alanine amino-transferase (ALT), glucose, tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), immunoglobin G (IgG), and C-reactive protein (CRP) levels compared to their levels in TiO2-NPs-treated rats. The aforementioned antioxidants also effectively modulated the changes in the levels of serum vascular endothelial growth factor (VEGF), nitric oxide (NO), hepatic DNA breakage, caspase-3, and inhibition of drug metabolizing enzymes (cytochrome P450s; CYP4502E12E1) in rat livers induced by TiO2-NPs toxicity. The histopathological examination of the liver section showed that TiO2-NPs caused severe degeneration of most hepatocytes with an increase in collagen in the portal region, while treatment with the antioxidants in question improved liver architecture. These outcomes supported the use of Qur and Id as protective agents against the hepatotoxicity induced by TiO2-NPs and other hepatotoxic drugs.

Exploration of cytotoxic and genotoxic endpoints following sub-chronic oral exposure to titanium dioxide nanoparticles

2019 ◽  
Vol 35 (9) ◽  
pp. 577-592 ◽  
Author(s):  
Srijita Chakrabarti ◽  
Danswrang Goyary ◽  
Sanjeev Karmakar ◽  
Pronobesh Chattopadhyay
Keyword(s):  
Titanium Dioxide ◽  
Titanium Dioxide Nanoparticles ◽  
Flow Cytometric Analysis ◽  
Raw 264.7 Cells ◽  
Oral Exposure ◽  
Chromosomal Breakage ◽  
Flow Cytometric ◽  
Higher Doses

Health hazards of titanium dioxide nanoparticles (TiO2-NPs) have raised severe concerns because of the paucity of information regarding the toxic effects among the population. In the present research, the in vitro and in vivo cytotoxic potential of TiO2-NPs were evaluated using flow cytometric techniques. Further, in vitro and in vivo genotoxic endpoints were estimated by means of comet, micronucleus (MN), and chromosomal aberration (CA) assays. In vitro analysis was performed at the concentration range of 10–100 µg/mL using murine RAW 264.7 cells. In vivo experiments were conducted on Albino mice (M/F) by exposing them to 200 and 500 mg/kg TiO2-NPs for 90 days. Decreased percentage of cell viability with higher doses of TiO2-NPs was evident in both in vitro and in vivo flow cytometric analysis. Further, an impaired cell cycle (G0/G1, S, and G2/M) was reflected in the present investigation following the exposure to TiO2-NPs. Increased comet scores such as tail length, % DNA in tail, tail moment, and olive moment were also observed with the higher doses of TiO2-NPs in vitro and in vivo comet assays. Finally, the in vivo MN and CA assays revealed the formation of MN and chromosomal breakage following the exposure to TiO2-NPs.

scholarly journals Agglomeration of titanium dioxide nanoparticles increases toxicological responses in vitro and in vivo

2020 ◽  
Vol 17 (1) ◽  
Author(s):  
Sivakumar Murugadoss ◽  
Frederic Brassinne ◽  
Noham Sebaihi ◽  
Jasmine Petry ◽  
Stevan M. Cokic ◽  
...  
Keyword(s):  
Titanium Dioxide ◽  
Titanium Dioxide Nanoparticles

Ameliorative Action of Curcumin in Cisplatin-mediated Hepatotoxicity: An In Vivo Study in Wistar Rats

2014 ◽  
Vol 45 (6) ◽  
pp. 462-468 ◽  
Author(s):  
Mohammad Waseem ◽  
Priyanka Pandey ◽  
Babita Tomar ◽  
Sheikh Raisuddin ◽  
Suhel Parvez
Keyword(s):  
Wistar Rats ◽  
In Vivo Study

scholarly journals Titanium dioxide nanoparticles exaggerate respiratory syncytial virus-induced airway epithelial barrier dysfunction

2020 ◽  
Vol 319 (3) ◽  
pp. L481-L496
Author(s):  
Carrie C. Smallcombe ◽  
Terri J. Harford ◽  
Debra T. Linfield ◽  
Susana Lechuga ◽  
Vladimir Bokun ◽  
...  
Keyword(s):  
Titanium Dioxide ◽  
Respiratory Syncytial Virus ◽  
Titanium Dioxide Nanoparticles ◽  
Airway Disease ◽  
Epithelial Barrier ◽  
Airway Epithelial ◽  
Barrier Dysfunction ◽  
Syncytial Virus ◽  
Epithelial Barrier Dysfunction

Respiratory syncytial virus (RSV) is the leading cause of lower respiratory tract infections in children worldwide. While most develop a mild, self-limiting illness, some develop severe acute lower respiratory infection and persistent airway disease. Exposure to ambient particulate matter has been linked to asthma, bronchitis, and viral infection in multiple epidemiological studies. We hypothesized that coexposure to nanoparticles worsens RSV-induced airway epithelial barrier dysfunction. Bronchial epithelial cells were incubated with titanium dioxide nanoparticles (TiO2-NP) or a combination of TiO2-NP and RSV. Structure and function of epithelial cell barrier were analyzed. Viral titer and the role of reactive oxygen species (ROS) generation were evaluated. In vivo, mice were intranasally incubated with TiO2-NP, RSV, or a combination. Lungs and bronchoalveolar lavage (BAL) fluid were harvested for analysis of airway inflammation and apical junctional complex (AJC) disruption. RSV-induced AJC disruption was amplified by TiO2-NP. Nanoparticle exposure increased viral infection in epithelial cells. TiO2-NP induced generation of ROS, and pretreatment with antioxidant, N-acetylcysteine, reversed said barrier dysfunction. In vivo, RSV-induced injury and AJC disruption were augmented in the lungs of mice given TiO2-NP. Airway inflammation was exacerbated, as evidenced by increased white blood cell infiltration into the BAL, along with exaggeration of peribronchial inflammation and AJC disruption. These data demonstrate that TiO2-NP exposure exacerbates RSV-induced AJC dysfunction and increases inflammation by mechanisms involving generation of ROS. Further studies are required to determine whether NP exposure plays a role in the health disparities of asthma and other lung diseases, and why some children experience more severe airway disease with RSV infection.

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