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Toxic response of graphene nanoplatelets in vivo and in vitro

Authors
Park, Eun-JungLee, Gwang-HeeHan, Beom SeokLee, Byoung-SeokLee, SominCho, Myung-HaingKim, Jae-HoKim, Dong-Wan
Issue Date
9월-2015
Publisher
SPRINGER HEIDELBERG
Keywords
Graphene; Nanoplatelets; Toxicity; Autophagy; Mitochondria
Citation
ARCHIVES OF TOXICOLOGY, v.89, no.9, pp.1557 - 1568
Indexed
SCIE
SCOPUS
Journal Title
ARCHIVES OF TOXICOLOGY
Volume
89
Number
9
Start Page
1557
End Page
1568
URI
https://scholar.korea.ac.kr/handle/2021.sw.korea/92645
DOI
10.1007/s00204-014-1303-x
ISSN
0340-5761
Abstract
With the development of nanotechnology, myriad types of novel materials have been discovered at the nanoscale, among which the most interesting material is graphene. However, the toxicity data available on graphene are extremely limited. In this study, we explored toxic response of commercially available graphene nanoplatelets (GNPs) in vivo and in vitro. The GNPs used in this study had a high surface area and feature considerably few defects. In mice, GNPs (2.5 and 5 mg/kg) remained in the lung until 28 days after a single instillation, and the secretion of inflammatory cytokines reached the maximal level at Day 14 and then decreased over time. In vitro study using BEAS-2B cells, a human bronchial epithelial cell line, GNPs located within autophagosome-like vacuoles 24 h after exposure. The GNPs (2.5, 5, 10, and 20 mu g/mL) also dose-dependently reduced cell viability, which was accompanied by an increase in the portion of cells in the subG1 and S phases. Moreover, the GNPs down-regulated the generation of reactive oxygen species, suppressed ATP production, caused mitochondria damage, and elevated the levels of autophagy-related proteins. Based on these results, we suggest that GNPs provoked a subchronic inflammatory response in mice and that GNPs induced autophagy accompanying apoptosis via mitochondria damage in vitro.
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