Genotoxicity, cytotoxicity, and reactive oxygen species induced by single-walled carbon nanotubes and C(60) fullerenes in the FE1-Mutatrade markMouse lung epithelial cells

Research output: Contribution to journalJournal articleResearchpeer-review

Standard

Genotoxicity, cytotoxicity, and reactive oxygen species induced by single-walled carbon nanotubes and C(60) fullerenes in the FE1-Mutatrade markMouse lung epithelial cells. / Jacobsen, Nicklas Raun; Pojana, Giulio; White, Paul; Møller, Peter; Cohn, Corey Alexander; Korsholm, Karen Smith; Vogel, Ulla; Marcomini, Antonio; Loft, Steffen; Wallin, Håkan.

In: Environmental and Molecular Mutagenesis, Vol. 49, No. 6, 2008, p. 476-87.

Research output: Contribution to journalJournal articleResearchpeer-review

Harvard

Jacobsen, NR, Pojana, G, White, P, Møller, P, Cohn, CA, Korsholm, KS, Vogel, U, Marcomini, A, Loft, S & Wallin, H 2008, 'Genotoxicity, cytotoxicity, and reactive oxygen species induced by single-walled carbon nanotubes and C(60) fullerenes in the FE1-Mutatrade markMouse lung epithelial cells', Environmental and Molecular Mutagenesis, vol. 49, no. 6, pp. 476-87. https://doi.org/10.1002/em.20406

APA

Jacobsen, N. R., Pojana, G., White, P., Møller, P., Cohn, C. A., Korsholm, K. S., Vogel, U., Marcomini, A., Loft, S., & Wallin, H. (2008). Genotoxicity, cytotoxicity, and reactive oxygen species induced by single-walled carbon nanotubes and C(60) fullerenes in the FE1-Mutatrade markMouse lung epithelial cells. Environmental and Molecular Mutagenesis, 49(6), 476-87. https://doi.org/10.1002/em.20406

Vancouver

Jacobsen NR, Pojana G, White P, Møller P, Cohn CA, Korsholm KS et al. Genotoxicity, cytotoxicity, and reactive oxygen species induced by single-walled carbon nanotubes and C(60) fullerenes in the FE1-Mutatrade markMouse lung epithelial cells. Environmental and Molecular Mutagenesis. 2008;49(6):476-87. https://doi.org/10.1002/em.20406

Author

Jacobsen, Nicklas Raun ; Pojana, Giulio ; White, Paul ; Møller, Peter ; Cohn, Corey Alexander ; Korsholm, Karen Smith ; Vogel, Ulla ; Marcomini, Antonio ; Loft, Steffen ; Wallin, Håkan. / Genotoxicity, cytotoxicity, and reactive oxygen species induced by single-walled carbon nanotubes and C(60) fullerenes in the FE1-Mutatrade markMouse lung epithelial cells. In: Environmental and Molecular Mutagenesis. 2008 ; Vol. 49, No. 6. pp. 476-87.

Bibtex

@article{b6846d90e93a11ddbf70000ea68e967b,
title = "Genotoxicity, cytotoxicity, and reactive oxygen species induced by single-walled carbon nanotubes and C(60) fullerenes in the FE1-Mutatrade markMouse lung epithelial cells",
abstract = "Viability, cell cycle effects, genotoxicity, reactive oxygen species production, and mutagenicity of C(60) fullerenes (C(60)) and single-walled carbon nanotubes (SWCNT) were assessed in the FE1-Mutatrade markMouse lung epithelial cell line. None of these particles induced cell death within 24 hr at doses between 0 and 200 microg/ml or during long-term subculture exposure (576 hr) at 100 microg/ml, as determined by two different assays. However, cell proliferation was slower with SWCNT exposure and a larger fraction of the cells were in the G1 phase. Exposure to carbon black resulted in the greatest reactive oxygen species generation followed by SWCNT and C(60) in both cellular and cell-free particle suspensions. C(60) and SWCNT did not increase the level of strand breaks, but significantly increased the level of FPG sensitive sites/oxidized purines (22 and 56%, respectively) determined by the comet assay. The mutant frequency in the cII gene was unaffected by 576 hr of exposure to either 100 microg/ml C(60) or SWCNT when compared with control incubations, whereas we have previously reported that carbon black and diesel exhaust particles induce mutations using an identical exposure scenario. These results indicate that SWCNT and C(60) are less genotoxic in vitro than carbon black and diesel exhaust particles.",
author = "Jacobsen, {Nicklas Raun} and Giulio Pojana and Paul White and Peter M{\o}ller and Cohn, {Corey Alexander} and Korsholm, {Karen Smith} and Ulla Vogel and Antonio Marcomini and Steffen Loft and H{\aa}kan Wallin",
note = "Keywords: Animals; Cell Cycle; Cell Line; Cell Proliferation; Cell Survival; Comet Assay; DNA Damage; DNA Mutational Analysis; Epithelial Cells; Fullerenes; Lung; Mice; Mutagenicity Tests; Nanotubes, Carbon; Reactive Oxygen Species",
year = "2008",
doi = "10.1002/em.20406",
language = "English",
volume = "49",
pages = "476--87",
journal = "Environmental and Molecular Mutagenesis",
issn = "0893-6692",
publisher = "Wiley",
number = "6",

}

RIS

TY - JOUR

T1 - Genotoxicity, cytotoxicity, and reactive oxygen species induced by single-walled carbon nanotubes and C(60) fullerenes in the FE1-Mutatrade markMouse lung epithelial cells

AU - Jacobsen, Nicklas Raun

AU - Pojana, Giulio

AU - White, Paul

AU - Møller, Peter

AU - Cohn, Corey Alexander

AU - Korsholm, Karen Smith

AU - Vogel, Ulla

AU - Marcomini, Antonio

AU - Loft, Steffen

AU - Wallin, Håkan

N1 - Keywords: Animals; Cell Cycle; Cell Line; Cell Proliferation; Cell Survival; Comet Assay; DNA Damage; DNA Mutational Analysis; Epithelial Cells; Fullerenes; Lung; Mice; Mutagenicity Tests; Nanotubes, Carbon; Reactive Oxygen Species

PY - 2008

Y1 - 2008

N2 - Viability, cell cycle effects, genotoxicity, reactive oxygen species production, and mutagenicity of C(60) fullerenes (C(60)) and single-walled carbon nanotubes (SWCNT) were assessed in the FE1-Mutatrade markMouse lung epithelial cell line. None of these particles induced cell death within 24 hr at doses between 0 and 200 microg/ml or during long-term subculture exposure (576 hr) at 100 microg/ml, as determined by two different assays. However, cell proliferation was slower with SWCNT exposure and a larger fraction of the cells were in the G1 phase. Exposure to carbon black resulted in the greatest reactive oxygen species generation followed by SWCNT and C(60) in both cellular and cell-free particle suspensions. C(60) and SWCNT did not increase the level of strand breaks, but significantly increased the level of FPG sensitive sites/oxidized purines (22 and 56%, respectively) determined by the comet assay. The mutant frequency in the cII gene was unaffected by 576 hr of exposure to either 100 microg/ml C(60) or SWCNT when compared with control incubations, whereas we have previously reported that carbon black and diesel exhaust particles induce mutations using an identical exposure scenario. These results indicate that SWCNT and C(60) are less genotoxic in vitro than carbon black and diesel exhaust particles.

AB - Viability, cell cycle effects, genotoxicity, reactive oxygen species production, and mutagenicity of C(60) fullerenes (C(60)) and single-walled carbon nanotubes (SWCNT) were assessed in the FE1-Mutatrade markMouse lung epithelial cell line. None of these particles induced cell death within 24 hr at doses between 0 and 200 microg/ml or during long-term subculture exposure (576 hr) at 100 microg/ml, as determined by two different assays. However, cell proliferation was slower with SWCNT exposure and a larger fraction of the cells were in the G1 phase. Exposure to carbon black resulted in the greatest reactive oxygen species generation followed by SWCNT and C(60) in both cellular and cell-free particle suspensions. C(60) and SWCNT did not increase the level of strand breaks, but significantly increased the level of FPG sensitive sites/oxidized purines (22 and 56%, respectively) determined by the comet assay. The mutant frequency in the cII gene was unaffected by 576 hr of exposure to either 100 microg/ml C(60) or SWCNT when compared with control incubations, whereas we have previously reported that carbon black and diesel exhaust particles induce mutations using an identical exposure scenario. These results indicate that SWCNT and C(60) are less genotoxic in vitro than carbon black and diesel exhaust particles.

U2 - 10.1002/em.20406

DO - 10.1002/em.20406

M3 - Journal article

C2 - 18618583

VL - 49

SP - 476

EP - 487

JO - Environmental and Molecular Mutagenesis

JF - Environmental and Molecular Mutagenesis

SN - 0893-6692

IS - 6

ER -

ID: 9910241