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The Antioxidant Activity of Cerium Oxide Nanoparticles is Size Dependant and Blocks Aβ 1‐42 ‐Induced Free Radical Production and Neurotoxicity
Author(s) -
Singh Neeraj,
Amateis Eric,
Mahaney James E,
Meehan Kathleen,
Rzigalinski Beverly A
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.624.2
Subject(s) - radical , electron paramagnetic resonance , chemistry , antioxidant , neurotoxicity , superoxide , hydroxyl radical , cerium oxide , cerium , nuclear chemistry , nanoparticle , photochemistry , particle size , biophysics , oxide , inorganic chemistry , biochemistry , organic chemistry , toxicity , nanotechnology , nuclear magnetic resonance , materials science , physics , biology , enzyme
We have demonstrated that a single 10 nM dose of cerium oxide nanoparticles (CeONP) with an average size of 10 nm, extends the lifespan & preserves neuronal function in brain cell cultures. We hypothesize that CeONP act as regenerative free radical scavengers. Here, we investigated the antioxidant activity of CeONP using EPR. Hydroxyl radicals ( . OH) were generated via Fenton's reaction. Superoxide radicals (O 2 .– ) were generated by irradiating a solution of riboflavin and DMPO with UV rays. CeONP (10 nm) completely quenched . OH & O 2 .– formation. CeONP with a particle size of 7 nm were less effective than 10 nm particles. We also examined the effect of Fe‐doped ceria (6% Fe), which was less effective than CeONP. The toxic fragment of Αβ, Αβ 1‐42 , produces free radicals & is hypothesized to be a contributory factor in Alzheimer's pathology. When incubated with spin trap Αβ 1‐42 (1mg/ml) generated a 6 line EPR spectra. Αβ 1‐42 –induced free radical production was completely blocked by CeONP (10 nm). We also examined the neuroprotective capacity of the 3 groups of CeONP using UV, H 2 O 2 , & Αβ 1‐42 challenge. In comparison to 7 nm CeONP, cell death induced by UV & H 2 O 2 was reduced more effectively by 10 nm CeONP, whereas Fe‐doping of CeONP abrogated antioxidant protection. Neuronal death associated with Αβ 1‐42 was reduced 65% by CEONP (10 nm). Our results suggest that 1) CeONP exhibit potent antioxidant activity, which is dependent on size, composition, & particle surface area and 2) CeONP protect neurons from free radical damage & Αβ 1‐42 toxicity.