Abstract

Carbon nanomaterials have the numerous applications in biomedical sciences and nanotechnology-based industries. Nanodiamonds due to their unique physico-chemical properties compared to other carbon nanomaterials are suggested to be better drug carriers or implant coating. Nevertheless, little is known about their short- and long-term toxicological effects on humans, other biological systems and surrounding environment. In the present study, we evaluated genotoxic and mutagenic potential of nanodiamond (particle size <10nm) in human lymphocytes in vitro. Starting from concentration of 50μg/ml, diamond nanopowder was cytotoxic, inhibited cell proliferation and induced apoptotic cell death. Nanodiamond-associated oxidative stress was revealed, the effect was dose-dependent and statistically significant. Nanodiamond-mediated DNA oxidative damage (8-oxoG level) and changes in chromatin stability was observed even at as low as 1μg/ml concentration, which was especially seen for DNA single strand breaks estimated with alkaline comet assay. In contrast, no induction of DNA double strand breaks (neutral comet assay) was documented after nanodiamond treatment. Nanodiamond at concentration of 10μg/ml was able to stimulate micronuclei production. Centromeric signals found in nanodiamond-induced micronuclei may be due to aneugenic activity of diamond nanopowder. Taken together, we showed that nanodiamond-mediated oxidative stress may contribute to DNA damage limiting nanodiamond biocompatibility.

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