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Mutagenesis Advance Access originally published online on November 13, 2007
Mutagenesis 2008 23(1):27-33; doi:10.1093/mutage/gem034
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© The Author 2007. Published by Oxford University Press on behalf of the UK Environmental Mutagen Society. All rights reserved. For permissions, please e-mail: journals.permissions@oxfordjournals.org.

Assessment of the genotoxicity of trichloroethylene and its metabolite, S-(1,2-dichlorovinyl)-L-cysteine (DCVC), in the comet assay in rat kidney

Philip Clay*

Syngenta Central Toxicology Laboratory, Alderley Park, Macclesfield, Cheshire, SK10 4TJ, UK

Trichloroethylene (TCE) has been reported to give a small, but significant, increase in renal tumours in the rat. These tumours were always associated with nephrotoxicity which is most likely caused by the metabolism of TCE to S-(1,2-dichlorovinyl)-L-cysteine (DCVC) which accumulates in the proximal tubules. The genotoxicity of TCE and DCVC have been evaluated in vivo using the comet assay to assess DNA breakage in the proximal tubules of rat kidneys. Rats were exposed to TCE by inhalation or to DCVC by oral gavage at dose levels in excess of those which produced effects in long-term bioassays. Cell suspensions were produced from proximal tubules isolated from the kidneys of treated rats and the level of DNA damage assessed in these cells using the pH >13 comet assay. In vitro and in vivo positive controls were included and demonstrated the sensitivity of the assay. TCE gave a clearly negative response in the assay at all dose levels as did DCVC at the 16-h sampling time and at the 2-h sampling time with the lower dose level. At the 2-h sampling time following administration of DCVC at the higher dose level (10 mg/kg), there was limited evidence of DNA damage in a small number of animals, but this was considered insufficient to indicate a positive response in this assay. These data support an overall conclusion, based on these and other published data, that the renal tumours seen in bioassays are non-genotoxic in origin.

* To whom correspondence should be addressed. Tel: +44 0 1625 515461; Email: phil.clay{at}mac.com

Received on October 19, 2006; revised on July 12, 2007; accepted on August 4, 2007.


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