Comparison of distribution and toxicity following repeated oral dosing of different vanadium oxide nanoparticles in mice.
Vanadium is an important ultra-trace element derived from fuel product combustion. With the development of nanotechnology, vanadium oxide nanoparticles (VO NPs) have been considered for application in various fields, thus the possibility of release into the environment and human exposure is also increasing. Considering that verification of bioaccumulation and relevant biological responses are essential for safe application of products, in this study, we aimed to identify the physicochemical properties that determine their health effects by comparing the biological effects and tissue distribution of different types of VO NPs in mice. For this, we prepared five types of VO NPs, commercial (C)-VO2 and -V2O5 NPs and synthetic (S)-VO2, -V2O3, and -V2O5 NPs. While the hydrodynamic diameter of the two types of C-VO NPs was irregular and impossible to measure, those of the three types of S-VO NPs was in the range of 125-170nm. The S- and C-V2O5 NPs showed higher dissolution rates compared to other VO NPs. We orally dosed the five types of VO NPs (70 and 210μg/mouse, approximately 2 and 6mg/kg) to mice for 28 days and compared their biodistribution and toxic effects. We found that S-V2O5 and S-V2O3 NPs more accumulated in tissues compared to other three types of VO NPs, and the accumulated level was in order of heart>liver>kidney>spleen. Additionally, tissue levels of redox reaction-related elements and electrolytes (Na(+), K(+), and Ca(2+)) were most clearly altered in the heart of treated mice. Notably, all S- and C-VO NPs decreased the number of WBCs at the higher dose, while total protein and albumin levels were reduced at the higher dose of S-V2O5 and S-V2O3 NPs. Taken together, we conclude that the biodistribution and toxic effects of VO NPs depend on their dissolution rates and size (surface area). Additionally, we suggest that further studies are needed to clarify effects of VO NPs on functions of the heart and the immune system.
Myunggok Eye Research Institute, Konyang University, Daejeon 302-718, South Korea. Electronic address: pejtoxic@hanmail.net.
Eun-Jung
EJ
Park
School of Civil, Environmental, and Architectural Engineering, Korea University, Seoul 136-713, South Korea.
Gwang-Hee
GH
Lee
Seoul Center, Korea Basic Science Institute, Seoul 126-16, South Korea.
Cheolho
C
Yoon
School of Civil, Environmental, and Architectural Engineering, Korea University, Seoul 136-713, South Korea. Electronic address: dwkim1@korea.ac.kr.
Dong-Wan
DW
Kim
D000818:Animals; D008297:Male; D053768:Metal Nanoparticles / Q000633:toxicity*; D051379:Mice; D008813:Mice, Inbred ICR; D010087:Oxides / Q000493:pharmacokinetics / Q000633:toxicity; D013047:Specific Pathogen-Free Organisms; D014018:Tissue Distribution; D014639:Vanadium / Q000493:pharmacokinetics / Q000633:toxicity*
D010087:Oxides; D014639:Vanadium
Distribution; Ion homeostasis; Redox reaction; Toxicity; Vanadium oxide nanoparticles