Oxidatively damaged DNA in rats exposed by oral gavage to C60 fullerenes and single-walled carbon nanotubes.
Cast your vote
You can rate an item by clicking the amount of stars they wish to award to this item.
When enough users have cast their vote on this item, the average rating will also be shown.
Your vote was cast
Thank you for your feedback
Thank you for your feedback
MetadataShow full item record
AbstractBACKGROUND: 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.
CitationEnviron. Health Perspect. 2009, 117 (5):703-708
SponsorsThis 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).
- Accumulation of lipids and oxidatively damaged DNA in hepatocytes exposed to particles.
- Authors: Vesterdal LK, Danielsen PH, Folkmann JK, Jespersen LF, Aguilar-Pelaez K, Roursgaard M, Loft S, Møller P
- Issue date: 2014 Jan 15
- Methanol exposure does not produce oxidatively damaged DNA in lung, liver or kidney of adult mice, rabbits or primates.
- Authors: McCallum GP, Siu M, Sweeting JN, Wells PG
- Issue date: 2011 Jan 15
- Dietary exposure to diesel exhaust particles and oxidatively damaged DNA in young oxoguanine DNA glycosylase 1 deficient mice.
- Authors: Risom L, Møller P, Dybdahl M, Vogel U, Wallin H, Loft S
- Issue date: 2007 Dec 10
- DNA damage in rats after a single oral exposure to diesel exhaust particles.
- Authors: Danielsen PH, Risom L, Wallin H, Autrup H, Vogel U, Loft S, Møller P
- Issue date: 2008 Jan 1
- Expression of human oxoguanine glycosylase 1 or formamidopyrimidine glycosylase in human embryonic kidney 293 cells exacerbates methylmercury toxicity in vitro.
- Authors: Ondovcik SL, Preston TJ, McCallum GP, Wells PG
- Issue date: 2013 Aug 15