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Alumina at 50 and 13 nm nanoparticle sizes have potential genotoxicity
Author(s) -
Zhang Qinli,
Wang Haiyang,
Ge Cuicui,
Duncan Jeremy,
He Kaihong,
Adeosun Samuel O.,
Xi Huaxin,
Peng Huiting,
Niu Qiao
Publication year - 2017
Publication title -
journal of applied toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.784
H-Index - 87
eISSN - 1099-1263
pISSN - 0260-437X
DOI - 10.1002/jat.3456
Subject(s) - genotoxicity , micronucleus test , comet assay , reactive oxygen species , dna damage , oxidative stress , micronucleus , chemistry , sperm , nanoparticle , ames test , biophysics , nanotoxicology , toxicology , microbiology and biotechnology , environmental chemistry , materials science , nanotechnology , biology , toxicity , biochemistry , genetics , dna , organic chemistry , bacteria , salmonella
Although nanomaterials have the potential to improve human life, their sideline effects on human health seem to be inevitable and still are unknown. Some studies have investigated the genotoxicity of alumina nanoparticles (AlNPs); however, this effect is still unclear due to insufficient evaluation and conflicting results. Using a battery of standard genotoxic assays, the present study offers evidence of the genotoxicity associated with aluminum oxide (alumina) at NP sizes of 50 and 13 nm, when compared with bulk alumina (10 μm). The genotoxicity induced by alumina at bulk and NP sizes was evaluated with Ames test, comet test, micronucleus assay and sperm deformity test. The mechanism related to the induction of reactive oxygen species was explored as well. Our results showed that AlNPs (13 and 50 nm) were able to enter cells and induced DNA damage, micronucleus in bone marrow, sperm deformation and reactive oxygen species induction in a time‐, dose‐ and size‐dependent manner. Therefore, we conclude that AlNPs (13 and 50 nm), rather than bulk alumina, induce markers of genotoxicity in mice, with oxidative stress as a potential mechanism driving these genotoxic effects. Copyright © 2017 John Wiley & Sons, Ltd.