Abstract

The cytotoxicity of ceria ultimately lies in its electronic structure, which is defined by the crystal structure, composition, and size. Despite previous studies focused on ceria uptake, distribution, biopersistance, and cellular effects, little is known about its chemical and structural stability and solubility once sequestered inside the liver. Mechanisms will be presented that elucidate the in vivo transformation in the liver. In vivo processed ceria reveals a particle-size effect towards the formation of ultrafines, which represent a second generation of ceria. A measurable change in the valence reduction of the second-generation ceria can be linked to an increased free-radical scavenging potential. The in vivo processing of the ceria nanoparticles in the liver occurs in temporal relation to the brain cellular and protein clearance responses that stem from the ceria uptake. This information is critical to establish a possible link between cellular processes and the observed in vivo transformation of ceria. The temporal linkage between the reversal of the pro-oxidant effect (brain) and ceria transformation (liver) suggests a cause-effect relationship.

Document Type

Article

Publication Date

8-2014

Notes/Citation Information

Published in Chempluschem, v. 79, no. 8, p. 1083-1088.

This is the peer reviewed version of the following article: Chempluschem, v. 79, no. 8, p. 1083-1088, which has been published in final form at http://dx.doi.org/10.1002/cplu.201402080. This article may be used for non-commercial purposes in accordance with Wiley-VCH Terms and Conditions for self-archiving.

Digital Object Identifier (DOI)

http://dx.doi.org/10.1002/cplu.201402080

Funding Information

The U.S. Environmental Protection Agency (EPA) is acknowledged for providing financial support (EPA Science to Achieve Results (STAR) Grant RD-833772 and Mr. Matt Hazzard for graphical design)

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