- DOI: 10.1039/9781849735476,10.1039/9781849735476-00257, ISBN: 978-1-84973-453-0 (print),978-1-84973-547-6 (e-book), ISSN: 1757-7136, URL: http://publications.jrc.ec.europa.eu/repository/handle/111111111/32809, URL: http://pubs.rsc.org/en/content/ebook/978-1-84973-453-0#!divbookcontent, JRC nr: JRC68591
- Publication date
- 1 October 2014
Under physiological conditions, cells maintain a reduced intracellular state. This process is the result of a balance between the levels of oxidized and reduced species present in the cell. Oxidizing substances can create an imbalance in this state, for example by depleting electrons from aqueous redox species or by acting like catalysts. The overall result is the decrease of antioxidants and/or an increase in the production of reactive oxygen species (ROS), a cellular condition which eventually evolves into inflammatory and cytotoxic responses. ROS include hydrogen peroxide and superoxide ions; antioxidants are molecules such as vitamin C and glutathione which scavenge the unwanted oxidants. Here we use literature in vitro data to describe the application of a theorerical model of oxidative stress based on an electron-transfer mechanism, for the prediction of ROS generation by oxide nanoparticles.3 The model predictions are confronted with numerous literature studies that employ in vitro assays to test the cellular toxicity of the following nanoparticles: Al2O3, CuO, CeO2, Fe2O3, Fe3O4, NiO, SiO2, TiO2 and ZnO. The calculated properties of oxide nanomaterials, which reflect their reactivity, can be used to guide the experimental design of in vitro toxicological and acellular tests as well as to interpret their outcomes.
BURELLO Enrico, WORTH Andrew
Royal Society of Chemistry. RSC