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Properties of disorder-engineered black titanium dioxide nanoparticles through hydrogenation.

ABSTRACT: The recent discovery of "black" TiO2 nanoparticles with visible and infrared absorption has triggered an explosion of interest in the application of TiO2 in a diverse set of solar energy systems; however, what a black TiO2 nanoparticle really is remains a mystery. Here we elucidate more properties and try to understand the inner workings of black TiO2 nanoparticles with hydrogenated disorders in a surface layer surrounding a crystalline core. Contrary to traditional findings, Ti(3+) here is not responsible for the visible and infrared absorption of black TiO2, while there is evidence of mid-gap states above the valence band maximum due to the hydrogenated, engineered disorders. The hydrogen atoms, on the other hand, can undergo fast diffusion and exchange. The enhanced hydrogen mobility may be explained by the presence of the hydrogenated, disordered surface layer. This unique structure thus may give TiO2, one of the most-studied oxide materials, a renewed potential.

SUBMITTER: Chen X

PROVIDER: S-EPMC3607837 | biostudies-other | 2013

REPOSITORIES: biostudies-other

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Properties of disorder-engineered black titanium dioxide nanoparticles through hydrogenation.

Chen Xiaobo X Liu Lei L Liu Zhi Z Marcus Matthew A MA Wang Wei-Cheng WC Oyler Nathan A NA Grass Michael E ME Mao Baohua B Glans Per-Anders PA Yu Peter Y PY Guo Jinghua J Mao Samuel S SS

Scientific reports 20130101

The recent discovery of "black" TiO2 nanoparticles with visible and infrared absorption has triggered an explosion of interest in the application of TiO2 in a diverse set of solar energy systems; however, what a black TiO2 nanoparticle really is remains a mystery. Here we elucidate more properties and try to understand the inner workings of black TiO2 nanoparticles with hydrogenated disorders in a surface layer surrounding a crystalline core. Contrary to traditional findings, Ti(3+) here is not ...[more]

PMID: 23528851

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Project description:BackgroundEpidemiological emerging evidence shows that human exposure to some nanosized materials present in the environment would contribute to the onset and/or progression of Alzheimer's disease (AD). The cellular and molecular mechanisms whereby nanoparticles would exert some adverse effects towards neurons and take part in AD pathology are nevertheless unknown.ResultsHere, we provide the prime evidence that titanium dioxide (TiO2) and carbon black (CB) nanoparticles (NPs) bind the cellular form of the prion protein (PrPC), a plasma membrane protein well known for its implication in prion diseases and prion-like diseases, such as AD. The interaction between TiO2- or CB-NPs and PrPC at the surface of neuronal cells grown in culture corrupts PrPC signaling function. This triggers PrPC-dependent activation of NADPH oxidase and subsequent production of reactive oxygen species (ROS) that alters redox equilibrium. Through PrPC interaction, NPs also promote the activation of 3-phosphoinositide-dependent kinase 1 (PDK1), which in turn provokes the internalization of the neuroprotective TACE α-secretase. This diverts TACE cleavage activity away from (i) TNFα receptors (TNFR), whose accumulation at the plasma membrane augments the vulnerability of NP-exposed neuronal cells to TNFα -associated inflammation, and (ii) the amyloid precursor protein APP, leading to overproduction of neurotoxic amyloid Aβ40/42 peptides. The silencing of PrPC or the pharmacological inhibition of PDK1 protects neuronal cells from TiO2- and CB-NPs effects regarding ROS production, TNFα hypersensitivity, and Aβ rise. Finally, we show that dysregulation of the PrPC-PDK1-TACE pathway likely occurs in the brain of mice injected with TiO2-NPs by the intra-cerebro-ventricular route as we monitor a rise of TNFR at the cell surface of several groups of neurons located in distinct brain areas.ConclusionOur in vitro and in vivo study thus posits for the first time normal cellular prion protein PrPC as being a neuronal receptor of TiO2- and CB-NPs and identifies PrPC-coupled signaling pathways by which those nanoparticles alter redox equilibrium, augment the intrinsic sensitivity of neurons to neuroinflammation, and provoke a rise of Aβ peptides. By identifying signaling cascades dysregulated by TiO2- and CB-NPs in neurons, our data shed light on how human exposure to some NPs might be related to AD.

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Properties of disorder-engineered black titanium dioxide nanoparticles through hydrogenation.

Publications

Properties of disorder-engineered black titanium dioxide nanoparticles through hydrogenation.

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