Electron Localization Determines Defect Formation on Ceria Substrates

Abstract

The high performance of ceria (CeO2) as an oxygen buffer and active support for noble metals in catalysis relies on an efficient supply of lattice oxygen at reaction sites governed by oxygen vacancy formation. We used high-resolution scanning tunneling microscopy and density functional calculations to unravel the local structure of surface and subsurface oxygen vacancies on the (111) surface. Electrons left behind by released oxygen localize on cerium ions. Clusters of more than two vacancies exclusively expose these reduced cerium ions, primarily by including subsurface vacancies, which therefore play a crucial role in the process of vacancy cluster formation. These results have implications for our understanding of oxidation processes on reducible rare-earth oxides.

Cerium oxide nanoparticles protect against Aβ-induced mitochondrial fragmentation and neuronal cell death

“…Nanoceria reduced the SNOC-induced increase in DRP1 S616 phosphorylation ( Figure 5a). Similarly, nanoceria or NAC abolished Ab [25][26][27][28][29][30][31][32][33][34][35] -induced DRP1 S616 phosphorylation ( Figure 5b). …”

“…Our data on mitochondrial localization of nanoceria are in agreement with recent findings in hepatocytes and organotypic hippocampal brain slices. 35,42 Here we report that nanoceria reduced in situ ROS/RNS, as visualized by decreasing APF oxidation ( Figure 2) and 3-nitrotyrosine (3-NT) nitration in both SNOC and Ab [25][26][27][28][29][30][31][32][33][34][35] stressed neurons (Figures 3a-c). This is important because increased levels of nitrated proteins have been reported in AD brains and cerebrospinal fluid of AD patients, 43 and numerous proteins in AD have been shown to be nitrated by peroxynitrite.…”

“…Values listed under blots represent relative ratios of p-DRP1 S616 to total DRP1 protein, normalized to actin. (b) Western blots of p-DRP1 S616, total DRP1 and actin protein levels from neurons exposed to nanoceria (100 nM) or pre-aggregated 10 mM Ab [25][26][27][28][29][30][31][32][33][34][35] alone or in combination for 6 h or a combination of NAC (50 mM; 3 h pretreatment) and Ab [25][26][27][28][29][30][31][32][33][34][35] . Values listed under blots represent relative ratios of p-DRP1 S616 to total DRP1 protein normalized to actin nanoparticles to cross the BBB strikingly increased after injury (resulting in increased ROS/RNS).…”

“…Oxidation of Ce 4 þ to Ce 3 þ causes oxygen vacancies and defects on the surface of the crystalline lattice structure of the nanoparticles, generating a cage for redox reactions to occur. 30 Accordingly, nanoceria mimic the catalytic activities of antioxidant enzymes, such as SOD 31,32 and catalase, 33 and are able to neutralize peroxynitrite. 34 Because of these antioxidant properties, we hypothesized that nanoceria could detoxify peroxynitrite and protect against Ab-induced DRP1 S616 hyperphosphorylation, mitochondrial fragmentation and neuronal cell death.…”

Cerium dioxide nanoparticles selectively up-regulate C-C chemokine receptor 2 and CD16 expression on human monocytes

“…CeO2 NPs can also behave as scavengers of reactive oxygen species (ROS) because of cerium autoregenerative cycle of its two oxidation states, Ce 3+ as Ce2O3 and Ce 4+ as CeO2. The presence of both Ce (III) / Ce (IV) valence forms and the oxygen vacancies on their surface (Esch, 2005;Fronzi, 2009) let these NPs store and release oxygen, being responsible for ceria catalytic and antioxidant properties. This specific property of the material stimulated research focused on CeO2 NPs for the development of biomedical systems and pharmacological treatments such as antioxidant therapy and radio-protection (Celardo, 2011).…”