Journal
JOURNAL OF PHYSICAL CHEMISTRY C
Volume 117, Issue 1, Pages 383-392Publisher
AMER CHEMICAL SOC
DOI: 10.1021/jp3101392
Keywords
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Funding
- National Basic Research Program (973 program) [2011CB933403, 2012CB930000]
- National Natural Science Foundation of China [10905064, 11275214, 10975148]
- FY11 FDA Nanotechnology CORES Program
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A wide range of nanoparticles (NPs) have been found to generate free radicals in biological systems. Hence, it is hypothesized that free radical generation may play a key role in the mechanism of nanomaterial toxicity in vivo. However, the main physicochemical basis for the free radical generation particularly in the biomicroenvironment has not yet been fully established. In this study, we performed comprehensive spectroscopic techniques to probe the physicochemical origin of free radical generation induced by iron oxide nanoparticles in biomicroenvironment. We demonstrated that alpha-Fe2O3 and gamma-Fe2O3 NPs induced hydroxyl radical ((OH)-O-center dot) via homogeneous and heterogeneous Fenton process, depending on the biological microenvironment of pH and reducing agent presence. The physicochemical structures such as chemical states of oxygen and iron on nanosurface are the key factors in the homogeneous and heterogeneous catalytic reactions. A noteworthy finding was that in situ surface reduction of Fe2O3 NPs occurred in the presence of a physiological amount of biological reducing agents (L-cysteine or NADPH), which could enhance and even reverse the capacity of (OH)-O-center dot generation by alpha-Fe2O3 and gamma-Fe2O3 NPs under low pH 1.2 condition. The present study demonstrates that exploration of the physicochemical basis at the nanobio interface in biomicroenvironments may help to understand the mechanism of nanotoxicity and guide safe design of nanomaterials for biomedical application
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