Toxicity and penetration of TiO2 nanoparticles in hairless mice and porcine skin after subchronic dermal exposure

Wu, Jianhong; Liu, Wei; Cheng, Xue; Zhou, Sanming; Lan, Fengli; Bi, Lei; Xu, Huibi; Yang, Xiangliang; Fan-dian, Zeng

doi:10.1016/j.toxlet.2009.05.020

Cited by 414 publications

(286 citation statements)

References 25 publications

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“…There are no published reports on TiO 2 -NM-controlled human exposures without any confounding factors over a long period of time and quantification of TiO 2 -NM accumulation in all the major organs. Mouse studies, however, involving respiratory and dermal introduction of TiO 2 -NM did show a low percentage (lung accumulation estimate of 0.003%) of traversing the various barriers to reach and accumulate in the major organs 21,22 . Occupational inhalation of manufactured TiO 2 -NM and its corresponding accumulation in the lungs is high with a comparatively low clearance rate 34 .…”

Section: Discussionmentioning

confidence: 94%

Titanium dioxide nanomaterials cause endothelial cell leakiness by disrupting the homophilic interaction of VE–cadherin

et al. 2013

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The use of nanomaterials has raised safety concerns, as their small size facilitates accumulation in and interaction with biological tissues. Here we show that exposure of endothelial cells to TiO 2 nanomaterials causes endothelial cell leakiness. This effect is caused by the physical interaction between TiO 2 nanomaterials and endothelial cells' adherens junction protein VE-cadherin. As a result, VE-cadherin is phosphorylated at intracellular residues (Y658 and Y731), and the interaction between VE-cadherin and p120 as well as b-catenin is lost. The resulting signalling cascade promotes actin remodelling, as well as internalization and degradation of VE-cadherin. We show that injections of TiO 2 nanomaterials cause leakiness of subcutaneous blood vessels in mice and, in a melanoma-lung metastasis mouse model, increase the number of pulmonary metastases. Our findings uncover a novel non-receptor-mediated mechanism by which nanomaterials trigger intracellular signalling cascades via specific interaction with VE-cadherin, resulting in nanomaterial-induced endothelial cell leakiness.

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Section: Discussionmentioning

confidence: 94%

Titanium dioxide nanomaterials cause endothelial cell leakiness by disrupting the homophilic interaction of VE–cadherin

et al. 2013

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“…However, smaller nanoparticles can penetrate skin and then undergo translocation to various organs. 11 After absorption, nanoparticles are carried by the bloodstream to various organs. Nanoparticles easily enter organs with high blood flow, such as the liver and spleen, and are retained effectively by the reticuloendothelial system (RES) of these organs.…”

Section: Absorption Distribution Metabolism and Excretion Of Nanopmentioning

confidence: 99%

Perturbation of physiological systems by nanoparticles

et al. 2014

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Nanotechnology is having a tremendous impact on our society. However, societal concerns about human safety under nanoparticle exposure may derail the broad application of this promising technology. Nanoparticles may enter the human body via various routes, including respiratory pathways, the digestive tract, skin contact, intravenous injection, and implantation. After absorption, nanoparticles are carried to distal organs by the bloodstream and the lymphatic system. During this process, they interact with biological molecules and perturb physiological systems. Although some ingested or absorbed nanoparticles are eliminated, others remain in the body for a long time. The human body is composed of multiple systems that work together to maintain physiological homeostasis. The unexpected invasion of these systems by nanoparticles disturbs normal cell signaling, impairs cell and organ functions, and may even cause pathological disorders. This review examines the comprehensive health risks of exposure to nanoparticles by discussing how nanoparticles perturb various physiological systems as revealed by animal studies. The potential toxicity of nanoparticles to each physiological system and the implications of disrupting the balance among systems are emphasized.

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“…They have been used as bactericidal agents in artificial heart valves (Jackson et al 2006). Many evidences suugested that TiO 2 nanoparticles taken by different routs could enter the heart causing toxicological effects, including the histopathological changes (Olmedo et al 2002;Wu et al 2009;Sheng et al 2013). The routs of cellular uptake are either endocytosis by active uptake, or passive diffusion (Geiser et al 2008).…”

Section: Discussionmentioning

confidence: 99%

Role of Carnosine and Melatonin in Ameliorating Cardiotoxicity of Titanium Dioxide Nanoparticles in the Rats

Al-Rasheed¹,

Faddah²,

Ibrahim

et al. 2015

Braz. arch. biol. technol.

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The aim of this work was to study the possible cardiotoxicity of two different doses of 50 nm nano titanium dioxide (n-TiO 2 ) and the possible modulating effects of the use of two natural antioxidants carnosine and melatonin. The results showed that TiO 2-NPs produced deleterious effects on rat cardiac tissue as confirmed by the increased levels of serum myoglobin, troponin-T and CK-MB. Increased levels of serum Inflammatory markers represented by the tumor necrosis factor alpha (TNF-α) and

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Toxicity and penetration of TiO2 nanoparticles in hairless mice and porcine skin after subchronic dermal exposure

Cited by 414 publications

References 25 publications

Titanium dioxide nanomaterials cause endothelial cell leakiness by disrupting the homophilic interaction of VE–cadherin

Titanium dioxide nanomaterials cause endothelial cell leakiness by disrupting the homophilic interaction of VE–cadherin

Perturbation of physiological systems by nanoparticles

Role of Carnosine and Melatonin in Ameliorating Cardiotoxicity of Titanium Dioxide Nanoparticles in the Rats

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