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Janne K. Folkmann,¹ Lotte Risom,¹ Nicklas R. Jacobsen,² Håkan Wallin,² Steffen Loft,¹ and Peter Møller¹

¹Institute of Public Health, Department of Environmental Health, University of Copenhagen, Copenhagen, Denmark; ²National Research Centre for the Working Environment, Copenhagen, Denmark

Abstract
Background: C₆₀ fullerenes and single-walled carbon nanotubes (SWCNT) are projected to be used in medicine and consumer products with potential human exposure. The hazardous effects of these particles are expected to involve oxidative stress with generation of oxidatively damaged DNA that might be the initiating event in the development of cancer.

Objective: In this study we investigated the effect of a single oral administration of C₆₀ fullerenes and SWCNT.

Methods: We measured the level of oxidative damage to DNA as the premutagenic 8-oxo-7,8-dihydro-2´-deoxyguanosine (8-oxodG) in the colon mucosa, liver, and lung of rats after intragastric administration of pristine C₆₀ fullerenes or SWCNT (0.064 or 0.64 mg/kg body weight) suspended in saline solution or corn oil. We investigated the regulation of DNA repair systems toward 8-oxodG in liver and lung tissue.

Results: Both doses of SWCNT increased the levels of 8-oxodG in liver and lung. Administration of C₆₀ fullerenes increased the hepatic level of 8-oxodG, whereas only the high dose generated 8-oxodG in the lung. We detected no effects on 8-oxodG in colon mucosa. Suspension of particles in saline solution or corn oil yielded a similar extent of genotoxicity, whereas corn oil per se generated more genotoxicity than the particles. Although there was increased mRNA expression of 8-oxoguanine DNA glycosylase in the liver of C₆₀ fullerene-treated rats, we found no significant increase in repair activity.

Conclusions: Oral exposure to low doses of C₆₀ fullerenes and SWCNT is associated with elevated levels of 8-oxodG in the liver and lung, which is likely to be caused by a direct genotoxic ability rather than an inhibition of the DNA repair system.

Key words: cancer, DNA damage, DNA repair, nanoparticle, oxidative stress. Environ Health Perspect 117:703–708 (2009) . doi:10.1289/ehp.11922 available via http://dx.doi.org/ [Online 12 November 2008]

Address correspondence to P. Møller, Institute of Public Health, University of Copenhagen, Øster Farimagsgade 5A, Building 5B, Second Floor, DK-1014 Copenhagen, Denmark. Telephone: 45-3532-7654. Fax: 45-3532-7686. E-mail: p.moller@pubhealth.ku.dk

This study was supported by grants from the Research Centre for Environmental Health, the Danish Research Councils, and the European Union (grant FP6-012912, NEST, Particle Risk) and ECNIS (Environmental Cancer Risk, Nutrition and Individual Susceptibility) a network of excellence operating within the European Union Sixth Framework Program, Priority 5: Food Quality and Safety (contract 513943) .

The authors declare they have no competing financial interests.

Received 11 July 2008 ; accepted 12 November 2008.